Obesity-Related Hypertension: Epidemiology, Pathophysiology, and Clinical Management

Theodore A. Kotchen1
The prevalence of obesity, including childhood obesity, is increasing worldwide. Weight gain
is associated with increases in arterial pressure, and it has been estimated that 6070% of
hypertension in adults is attributable to adiposity. Centrally located body fat, associated with
insulin resistance and dyslipidemia, is a more potent determinant of blood pressure elevation
than peripheral body fat. Obesity-related hypertension may be a distinct hypertensive phenotype
with distinct genetic determinants. Mechanisms of obesity-related hypertension include insulin
resistance, sodium retention, increased sympathetic nervous system activity, activation of renin
angiotensinaldosterone, and altered vascular function. In overweight individuals, weight loss
results in a reduction of blood pressure, however, this effect may be attenuated in the long term.
An increasing number of community-based programs (including school programs and worksite
programs) are being developed for the prevention and treatment of obesity. Assessment and
treatment of the obese hypertensive patient should address overall cardiovascular disease (CVD)
risk. There are no compelling clinical trial data to indicate that any one class of antihypertensive
agents is superior to others, and in general the principles of pharmacotherapy for obese
hypertensive patients are not different from nonobese patients. Future research directions might
include: (i) development of effective, culturally sensitive strategies for the prevention and
treatment of obesity; (ii) clinical trials to identify the most effective drug therapies for reducing
CVD in obese, hypertensive patients; (iii) continued search for the genetic determinants of the
obese, hypertensive phenotype.
Masalah obesitas, mencakup obesitas pada masa kanak-kanak, sedang meningkat di seluruh
dunia. Kelebihan Berat badan dihubungkan dengan peningkatan tekanan di dalam urat nadi dan
telah diperkirakan bahwa 6070% berkaitan dengan hipertensi. Mekanisme hipertensi terkait
dengan obesitas meliputi pembalasan hormon insulin, sodium ingatan, meningkatnya aktivitas
sistem nerves simpatik, pengaktifan tentang reninangiotensinaldosterone, dan mengubah
fungsi vaskuler. Riset masa depan mungkin meliputi: ( i) pengembangan tentang strategi efektif,
secara cultural sensitip untuk pencegahan dan perawatan obesitas; ( ii) percobaan klinis untuk
mengidentifikasi therapy obat yang baik untuk mengurangi (CVD) pada obesitas, hypertensive
pasien; ( iii) dan dilanjutkan mencari faktor penentu keturunan untuk obesitas, hypertensive
phenotype.
Keywords: adipokines; blood pressure; central obesity; hypertension;
insulin resistance
American Journal of Hypertension, advance online publication 12 August 2010;
doi:10.1038/ajh.2010.172

Obesity is associated with increased morbidity and mortality due to hypertension, diabetes,
dyslipidemia, and cardiovascular and renal diseases.13 The prevalence of obesity and obesityrelated disease is increasing worldwide. The Centers for Disease Control and Prevention
estimated that obesity cost the United States at least $147 billion in 2008. Consequently,
strategies for preventing and treating obesity have become political as well as health-care issues.
Obesitas dihubungkan dengan angka kematian dan keadaan tidak sehat yang ditingkatkan
dalam kaitan dengan hipertensi, kencing manis, dyslipidemia, dan cardiovascular dan diseases.
Pusat pengendalian Dan Pencegahan penyakit memperkirakan bahwa obesitas di Amerika
Serikat sedikitnya berharga $ 147 milyar (Am.) 2008. Sebagai konsekwensi, strategi untuk
mencegah obesitas sudah menjadi politis seperti halnya isu pelayanan kesehatan.
Scientific and medical interest in the relationship between obesity and hypertension is
reflected in the number of publications related to this topic. The number of English language
citations in PubMed for obesity AND hypertension progressively increased from 203 in 1990
to 1,427 in 2009, with most of the increase occurring in the past decade. The purpose of this
report is to review information about the epidemiology, pathogenic mechanisms, and strategies
for prevention and treatment of obesity-related hypertension.
Secara medis dan ilmiah di dalam hubungan antara obesitas dan hipertensi dicerminkan
banyaknya penerbitan yang topik ini. Banyaknya kutipan Bahasa Inggris di dalam PubMed
Untuk obesitas dan hipertensi yang semakin meningkat dari 203 1990 menjadi 1,427 2009,
tujuan laporan ini adalah untuk meninjau ulang informasi tentang epidemiologi, mekanisme
pathogenic, dan strategi untuk pencegahan dan perawatan tentang hipertensi terkait dengan
obesitas.
Epidemiology of Obesity and Hypertension
In both adults and children, obesity rates have increased over the past several decades in the
United States.4,5 Obesity rates have increased in both genders, and among all racial, ethnic, and
socioeconomic groups. Approximately 68% of US adults are either overweight or obese.6 Based
on National Healthand Nutrition Examination Survey data, the prevalence of obesity in 2007
2008 was 32.2% among adult men and 35.5% among adult women.5 Among adults, the
prevalence of obesity increases with age in men. The prevalence of obesity among African
Americans is ~1.5 times that in whites, and Mexican Americans have an intermediate
prevalence.4
Epidemiologi Obesitas Dan Hipertensi
Pada orang dewasa dan anak-anak, rata-rata kegendutan sudah meningkat beberapa dekade
lalu di amerika serikat. Rata-rata tingkat kegendutan yang diperhitungkan sudah meningkat pada
kedua jenis kelamin, dan antar semua ras, kesukuan dan kelompok ekonomi-sosial, yang kirakira 68% orang dewasa AS adalah kelebihan berat/obese. berdasar pada Kesehatan Nasional dan
Data Survei Pengujian Ilmu gizi, kegendutan pada 20072008 adalah 32.2% orang orang dewasa
pria dan 35.5% orang dewasa wanita

During the past three decades, prevalence rates of childhood and adolescent obesity (body
mass index (BMI) >95th percentile for age and sex) have more than doubled in the United
States.7 In 2006, 16.3% of children and adolescents were reportedly obese,8 and ~32% of
children are either overweight or obese.6 Childhood obesity frequently persists into adulthood,
with up to 80% of obese children reported to become obese adults.9 Among adolescents, the
prevalence of obesity is approximately twice as high among African Americans and Mexican
Americans than among non-Hispanic whites.7
Pada tiga dekade yang lalu, obesitaspadat masa kanak-kanak dan anak remaja memiliki
(BMI) > 95th bagian perseratus untuk umur dan jenis kelamin. pada 2006, 16.3% anak-anak dan
remaja dilaporkan obesitas, dan ~ 32% anak-anak yang kelebihan berat atau obese. obesitas
pada masa asa kanak-kanak sering tetap berlanjut hingga dewasa, dengan rincian 80% anak-anak
yang gemuk saat dewasa menjadi obesitas.
Because of the increasing prevalence of obesity in the United States, it has been projected that
the steady increase in life expectancy during the past two centuries will soon end.10 However,
recent reports from the Centers for Disease Control and Prevention suggest that obesity rates
may be stabilizing.5,11 Obesity rates have remained constant for 5 years in men and closer to 10
years in women and children.
Laporan terbaru dari Pusat Pencegahan dan Pengendalian Penyakit menyatakan bahwa
obesitas mungkin akan stabil. Obesitas sudah menetap 5 tahun pada orang dan 10 tahun pada
wanita dan anak-anak.
The prevalence of obesity is increasing not only in the United States, but also globally.12,13
Socioeconomic and demographic transitions occurring in many developing countries are
contributing to the escalation of obesity despite continuing nutritional deficiencies. This double
burden poses health and economic challenges in resource-constrained populations. In 1998, the
prevalence of obesity in the developing world had increased from 2.3 to 19.6% over a 10-year
period.14 Obesity rates have increased threefold or more since 1980 in the Middle East, the
Pacific Islands, Australasia, and China. Additionally, the prevalence of childhood overweight has
increased in almost all countries for which data are available.15 Obesity in the developing world
is no longer a disease of higher socioeconomic status groups; the burden of obesity is shifting
toward groups with lower socioeconomic status as the countrys gross national product
increases.16 The increasing prevalence of obesity is related to urbanization, major changes in the
food supply, diet, and a reduction in physical activity.12,14
Obesitas yang meningkat tidak hanya terdapat di amerika serikat, tetapi juga global.
ekonomi-sosial dan transisi demografis yang terjadi di banyak negara berkembang menyokong
peningkatan obesitas. Pada 1998 obesitas di dunia meningkat dari 2.3 menjadi 19.6% dalam
periode 10 tahun .Obesitas sudah meningkat tiga kali lipat atau lebih sejak 1980 di timur
tengah, Pulau Pacific, Australia, dan Negeri China. Meningkatnya obesitas dihubungkan dengan
urbanisasi, perubahan utama di dalam persediaan makanan, diet, dan suatu pengurangan aktifitas
fisik

In parallel with increasing obesity rates, cardiovascular disease (CVD) mortality is rapidly
increasing in developing countries.17 Between 1990 and 2020, mortality from ischemic heart
disease and cerebrovascular disease increased to a considerably greater extent in developing than
in developed countries (Table 1). It is projected that by 2020, low- and middle- income countries
will contribute 19 million of the annual global mortality of 25 million due to CVD.12
Tabel 1 ,angka kematian global menaksir (dalam ribuan) penyakit jantung ischemic dan penyakit
cerebrovascular , berdasarkan jenis kelamin, antara 1990 dan 2020

Penyakit jantung iskemik

Negara berkembang
Negara maju
Penyakit cerebrovaskular
Negara berkembang
Negara maju

1990

Women
2020

%peningkatan

1990

Men
2020

%peningkatan

1,737
1,397

3,825
1,809

120
29

1,8282
1,297

4,337
1,921

137
48

1,499
867

3,100
1,113

107
28

1,454
539

3,260
841

124
56

Diadaptasi dari referen 17

Di dalam paralel dengan tingkat obesitas yang terus meningkat, penyakit cardiovascular
(CVD) dengan cepat terus meningkat dan berkembang. Antara 1990 dan 2020, angka kematian
dari penyakit jantung iskemik dan penyakit cerebrovascular dapat meningkat dengan sangat
luas dan lebih besar. ( Tabel 1) Itu diproyeksikan pada 2020, yang rendah- dan pertengahanpendapatan negara-negara akan menyokong 19 juta angka kematian, yang global tahunan 25 juta
dalam kaitan dengan (CVD).
Cross-sectional and longitudinal studies document an association of blood pressure with body
weight and an association of blood pressure increases over time with weight gain,1821 even
among lean individuals.22 However, the association of indices of adiposity with blood pressure
is less apparent among hypertensive individuals than among the general population,23
suggesting that the blood pressureadiposity relationship in hypertensives is modulated by
environmental and genetic factors. Nevertheless, obese individuals have a 3.5- fold increased
likelihood of having hypertension;19,24) 60% of hypertensive adults are >20% overweight. It
has been estimated that 6070% of hypertension in adults may be directly attributable to

adiposity.19 Possibly related to the increased prevalence of obesity, in US adults the prevalence
of hypertension increased from 25.0 to 28.7% between 19881991 and 19992000.25 Between
19881994 and 20072008, the prevalence of both obesity and hypertension increased among all
age groups of adults, although percentage increases of both were greatest among young adults
(Table 2).

Tabel 2| Obesitas dan hipertensi di Amerika Serikat pada dua periode waktu, dan persen peningkatannya

Umur
18 - 39
40 59
>60

% Hipertensi
198820051991
2006
5.1
7.4
27.0
32.1
57.9
65.8

%peningkat
an

45
19
14

% Obesitas
198820051994
2008
17.2
28.7
28.0
35.5
23.9
34.0

%peningkata
n

67
27
42

Data Survei Pengujian Ilmu gizi Dan Kesehatan Nasional Yang didasarkan memperoleh dari acuan 25
dan Pusat yang berikut untuk Kendali Penyakit Dan Lokasi Web Pencegahan: Www.Cdc.Gov/
Nchs/Nhanes/Nhanes2007-2008/Nhanes07_08.Htm Dan Www.Cdc.Gov/Nchs/Nhanes/Nh3Data.Htm.
Hipertensi= tekanan darah systolic > 140 Mm Hg atau tekanan darah diastolic > 90 mm Hg, atau
mengambil antihypertensive pengobatan. Obesitas= Badan berkumpul index > 30 kg/m2.

Cross-Sectional dan dokumen studi adalah suatu asosiasi tentang tekanan darah dengan
menimbang badan dan suatu asosiasi tentang tekanan darah yang meningkat dari waktu ke
waktu. Meskipun demikian, individu yang obesitas mempunyai 3.5- kali lipat kemungkinan
mempunyai hypertensi; 60% tentang hypertensi orang dewasa adalah > 20% kelebihan berat.
Pada orang dewasa AS hipertensi meningkat dari 25.0 menjadi 28.7% antara 19881991 dan
19992000.25 Antara 19881994 dan 20072008, tentang obesitas dan hipertensi meningkat
antar semua kelompok umur orang dewasa, walaupun peningkatan persentase kedua-duanya
terbesar antar orang dewasa muda ( Tabel 2).
Similar to adults, the prevalence of hypertension is threefold higher in obese children than in
nonobese children.26 Blood pressures in children have increased in the past decade, and this may
also be attributable, at least in part, to an increased prevalence of overweight.26,27 Additionally,
longitudinal studies document that weight gain is associated with increases in blood pressure and
hypertension incidence. For example, in the Framingham Heart Study, a 5% weight gain was
associated with a 2030% increase in hypertension incidence, and the Harvard Male Alumni
study found a weight gain of 25 pounds was associated with a 60% increase in hypertension
incidence.28,29

Serupa dengan orang dewasa, hipertensi tiga kali lipat lebih tinggi diderita anak-anak gemuk
dibanding anak yang tidak obese. apalagi, studi dokumen yang menimbang keuntungan
dihubungkan dengan peningkatan dalam tekanan darah dan timbulnya hipertensi. Sebagai
contoh, di dalam Framingham Studi Hati, suatu 5% keuntungan berat/beban telah dihubungkan
dengan suatu 2030% meningkat timbulnya hipertensi,dan Harvard Alumni Studi menemukan
suatu keuntungan berat/beban 25 pon telah dihubungkan dengan suatu 60% meningkat insiden
hipertensi .
Visceral obesity or android obesity is in part hormonally determined. Body fat distribution
is also affected by environmental and genetic factors. Environmental factors include alcohol
intake, cigarette smoking, and the timing of onset of childhood obesity.30 Most studies suggest
that centrally located body fat is a more important determinant of blood pressure elevation than
peripheral body fat in both men and women.3133 The relationship between waisthip ratio and
blood pressure appears to be independent of BMI.34 Visceral obesity also increases the risks for
insulin resistance and dyslipidemia. Further, insulin resistance and obesity are associated with
vascular endothelial dysfunction, manifested by endothelium- dependent coronary and peripheral
vasodilation.35,36 Impaired vasoreactivity, which may represent the initiation or early phase in
the evolution of atherosclerosis, is more strongly correlated with abdominal obesity than with
BMI.36
Badan gemuk juga dipengaruhi oleh lingkungan dan faktor keturunan. Faktor lingkungan
meliputi masukan alkohol, rokok bagi yang merokok, dan berbadan gemuk saat anak-anak.
Kebanyakan studi menyatakan badan yang gemuk adalah suatu faktor penentu tingginya tekanan
darah. Kegendutan mendalam juga meningkatkan resiko karena pembalasan hormon insulin dan
dyslipidemia. Lebih lanjut, pembalasan hormon insulin dan obesitas dihubungkan dengan
endothelial kelainan fungsi tubuh vaskuler, yang dinyatakan oleh endothelium- serangan jantung
bergantung dan vasodilation
The constellation of centripetal obesity (measured as waist circumference), hypertension,
insulin resistance, high serum triglyceride concentrations, and low levels of high-density
lipoprotein cholesterol constitutes the metabolic syndrome. This syndrome may be heritable,
but as shown in the rodent, it may be induced by diets high in simple carbohydrates.37 In African
Americans, we have found that insulin resistance is associated with blood pressure levels and
hypertension in men, but not in women, possibly reflecting the difference between android and
gynecoid obesity.38 In children and adolescents, the prevalence of the metabolic syndrome
increases with the severity of obesity, and approaches 50% in severely obese youngsters.39
Although the metabolic syndrome is associated with increased risk of all cause and
cardiovascular morbidity and mortality, whether the designation of a syndrome provides more
risk information than the individual risk factors by themselves has been questioned.4042
Peta bintang tentang obesitas bergerak menuju pusat ( yang diukur seperti lingkar pinggang),
hipertensi, pembalasan hormon insulin, serum tinggi triglyceride konsentrasi, dan untuk tingkat
rendah high-densas lipoprotein cholesterol mendasari sindrom yang berkenaan dengan
metabolisme. Sindrom ini mungkin turun temurun, tetapi seperti ditunjukkan binatang pengerat,
mungkin jadilah dibujuk oleh diet tinggi carbohydrates. Walaupun sindrom yang berkenaan

dengan metabolisme dihubungkan dengan meningkatnya resiko dari semua penyebab dan dapat
meningkatkan angka kematian dan keadaan cardiovascular yang tidak sehat
Evidence for a genetic contribution to both rare monogenic and to common forms of obesity
has recently been reviewed.43 Most genes that have been found to contribute to the pathogenesis
of obesity are expressed in the brain and appear to exert their effects by modulation of feeding
behavior. Obesityrelated hypertension may represent a genetically distinct hypertensive
phenotype. For example, some genes associated with adiposity may also contribute to the
development ofhypertension in overweight and obese individuals, e.g., tumor necrosis factor-,
3-adrenergic receptor, and G-protein 3 subunit.44 In a relatively isolated French Canadian
population, in 120 extended families with at least one sib pair affected with early onset
hypertension and/or dyslipidemia, a total genome scan identified a cluster of overlapping
quantitative trait loci with significant logarithm (base 10) of odds scores on chromosome 1 for
the following phenotypes: BMI, fasting insulin, leptin, diastolic blood pressure.45 Nevertheless,
to date, specific genetic factors have not been identified to account for the high heritabilities of
hypertension and/or obesity.
Tabel 3| Mekanisme yang bereputasi baik terkait hipertensi dan obesitas

Mekanisme utama

Mekanisme yang mendasari

Ingatan Sodium

Efek hormon insulin Antinatriuretic

Meningkatnya aktifitas ginjal SNS
Aldosterone yang meningkat
Aktifitas Cortisol yang meningkat
Tekanan Anatomic pada ginjal
Insulin resistance
Reninangiotensin
Leptin adipokines
Obstructive sleep apnea
Adrenergic receptor
polymorphisms
Psychological stress

Meningkatnya aktifitas SNS

Meningkatnya sirkulasi renin-angiotensin

Meningkatnya aktifitas ginjal SNS

Meningkatnya adipose renin-angiotensin

Lemahnya fungsi vascular endothelial

Insulin resistance

Mekanisme lain vaskuler

Insulin resistance
Altered vascular ion transport

SNS, Sympathetic Nervous System

Obesitas yang berhubungan dengan hipertensi boleh menghadirkan suatu hypertensive

phenotype yang beda. Sebagai contoh, beberapa gen berhubungan dengan adiposas boleh juga
berperan untuk pengembangan hipertensi di (dalam) individu gemuk sekali dan kelebihan berat,
e.g., tumor necrosis faktor-, sel yang peka rangsangan 3-adrenergic, dan G-Protein 3
subunit. Di Perancis yang terisolasi Populasi Kanada, pada 120 keluarga dengan sedikitnya satu
kaum keluarga menderita gejala awal hipertensi atau dyslipidemia. Meskipun demikian, sampai

saat ini, faktor spesifik keturunan belum dikenali untuk meliputi tingginya hipertensi dan
obesitas
Pathophysiology of Obesity-Related Hypertension
Environmental (e.g.diet content, physical activity, level of stress), physiological, and
genetic factors influence the impact of obesity on arterial pressure. An understanding of the
mechanisms of obesity-related hypertension may have important therapeutic implications. The
putative physiologic mechanisms of obesity-related hypertension are complex, interdependent,
and redundant (Table 3).

Patofisiologi dari Hipertensi Terkait dengan obesitas

Lingkungan ( e.g.diet isi, aktivitas fisik, tingkat tekanan), fisiologis, dan faktor keturunan
mempengaruhi dampak obesitas seperti tekanan urat arteri. Suatu pemahaman mekanisme dari
hipertensi terkait dengan kegendutan mungkin punya implikasi pengobatan yang penting.
fisiologi yang bereputasi baik mekanisme tentang hipertensi terkait dengan obesitas adalah
kompleks, saling tergantung, dan berlebihan (Tabel 3).
Sympathetic nervous system
Depending on populations studied and methods of measurement, most evidence indicate that
sympathetic nervous system activity is increased in obesity, particularly sympathetic activity to
the kidney and skeletal muscle, as measured by regional norepinephrine kinetic studies and
microneurography, respectively.4648 Neural activity to skeletal muscle is more closely related
to abdominal visceral fat than to total fat mass or abdominal subcutaneous fat.47 However,
hypertension is not an invariable consequence of obesity-related increases of neural activity.
Neural activity to the kidney and skeletal muscle is elevated in obese normotensive, as well as in
obese hypertensive humans.46,47 These observations raise the possibility that the impact of
obesity-related neural activity on arterial pressure is modified by environmental and genetic
factors, including race and gender. For example, muscle sympathetic nerve activity is primarily
related to BMI in men, but to blood pressure in women.49 In Pima Indians, despite a high
prevalence of obesity, muscle sympathetic nerve activity is low.49,50 This may provide a clue
for the relatively low prevalence of hypertension in Pima Indians.
Sistem nerves simpatik
kebanyakan bukti menunjukkan bahwa aktifitas sistem nerves simpatik meningkat pada
obesitas, terutama sekali aktifitas simpatik kepada ginjal dan otot. Bagaimanapun, hipertensi
bukanlah suatu konsekwensi yang tidak berubah-ubah dari peningkatan terkait dengan obesitas
tentang neural aktivitas. Sebagai contoh, aktifitaS otot saraf simpatik terutama semata
dihubungkan dengan BMI pada kebanyakan orang. Pada orang Pima indian, di samping suatu
tinggi obesitas, aktivitas otot syaraf simpatik adalah rendah. Ini merupakan suatu tanda hipertensi
rendah pada orang Pima indian.
The causes for activation of the sympathetic nervous system in obesity remain uncertain and
may be multiple.49 Putative mechanisms include hyperinsulinemia and/or insulin resistance;

leptin or other adipokines; reninangiotensin; lifestyle factors. Additionally, obesity, especially

upper body obesity, is a risk factor for obstructive sleep apnea. Hypertension is causally related
to sleep apnea, possibly due to sympathetic outflow as a consequence of intermittent hypoxia.51
Penyebab untuk pengaktifan sistem saraf yang simpatik pada obesitas tidak-pasti dan
mungkin adalah multiple. mekanisme meliputi hyperinsulinemia dan/atau pembalasan hormon
insulin; leptin atau lain adipokines; reninangiotensin; factor gaya hidup. Hipertensi oleh sebab
yang dihubungkan dengan tidur apnea, yang mungkin dalam kaitan dengan outflow simpatik
sebagai konsekwensi dari hypoxia.

Renal and adrenal mechanisms

Obesity-related hypertension is associated with renal sodium retention and impaired pressure
natriuresis.52 Obese humans and subjects with the metabolic syndrome tend to be relatively salt
sensitive.53,54 Increased renal tubular reabsorption of sodium has been attributed to increased
sympathetic outflow to the kidney. In the dog, renal denervation blunts sodium retention and
attenuates the rise in blood pressure associated with dietary-induced obesity. It has also been
suggested that increased intrarenal pressures caused by fat surrounding the kidneys and increased
abdominal pressure associated with visceral obesity may impair natriuresis.
Mekanisme Renal dan Adrenal
Hipertensi terkait dengan obesitas dihubungkan dengan sodium yang berkenaan dengan ginjal
dan tekanan natriuresis yang lemah. Manusia yang obesitas cenderung untuk menjadi secara
relative dan sensitive. kenaikan itu dalam tekanan darah berhubungan dengan obesitas dietaryinduced. telah diusulkan pula bahwa tekanan intrarenal yang ditingkatkan disebabkan oleh
kegemukan yang melingkupi ginjal dan meningkatnya tekanan abdominal.
Impaired pressure-natriuresis may also be related to increased mineralocorticoid activity. We
and others have reported that plasma aldosterone is associated with blood pressure, BMI, waist
circumference, and insulin resistance.5558 Among African Americans, aldosterone is
independently associated with hypertension, and plasma aldosterone concentrations are relatively
high in African Americans with the metabolic syndrome.57 These observations suggest that the
mineralocorticoid action of aldosterone contributes to obesityrelated hypertension, particularly
among African Americans. Consistent with a pathogenic role for aldosterone, the
mineralocorticoid antagonist, eplerenone, attenuates sodium retention and hypertension
associated with the development of obesity in dogs fed a high-fat diet.59 Somewhat
paradoxically, plasma aldosterone concentrations in obese and hypertensive African Americans
are relatively high despite low plasma renin activity. The stimulus for increased aldosterone
remains a matter of conjecture, however, recent reports indicate that adipokines may directly
stimulate aldosterone production.60
konsisten Dengan suatu peran pathogenic untuk aldosterone, mineralocorticoid, eplerenone,
menipis ingatan sodium dan hipertensi berhubungan dengan pengembangan obesitas di amerika

memberi makan suatu high-fat diet. Sedikit banyaknya secara bertentangan, plasma aldosterone
konsentrasi pada obesitas dan hypertensive Orang Amerika Dari Afrika secara relatif tinggi di
samping plasma rendah renin aktivitas. Stimulus untuk aldosterone yang ditingkatkan tinggal
suatu perihal tentang dugaan, bagaimanapun, laporan terbaru menunjukkan bahwa adipokines
boleh secara langsung merangsang produksi aldosterone
Although not as potent a mineralocorticoid as aldosterone, in high concentrations, cortisol
may increase arterial pressure by activating the mineralocorticoid receptor. Circulating levels of
cortisol are variable in obesity; however, they may not reflect cortisols activity in target
tissues.57 11-Hydroxysteroid dehydrogenase type 1 activates cortisone (a functionally inert
glucocorticoid) to cortisol (an active glucocorticoid) in target tissues, including adipose tissue.
This conversion is more pronounced in visceral than in subcutaneous adipose tissue.61 The P2HSD1 mouse with overexpression of HSD1 develops hypertension, features of the clinical
metabolic syndrome, and activation of the circulating reninangiotensinaldosterone system.62
Although these observations are provocative, a role for cortisol in the pathogenesis of obesityrelated hypertension and the metabolic syndrome remains to be established.
Walaupun bukan kuat, sebagai suatu mineralocorticoid aldosterone, pada konsentrasi tinggi,
cortisol dapat meningkatkan tekanan urat nadi dengan mengaktipkan mineralocorticoid sel yang
peka rangsangan. 11-Hydroxysteroid dehydrogenase mengetik 1 mengaktipkan kelenjar hormon
ke cortisol ( suatu glucocorticoid aktip) pada target jaringan/tisu, mencakup adipose. P2-Hsd1
Tikus dengan overexpression HSD1 berkembangnya hipertensi, corak sindrom berkenaan
dengan metabolisme yang klinis, dan pengaktifan sirkulasi reninangiotensinaldosterone
system.
Activation of the reninangiotensin system may also contribute to obesity-related
hypertension. Several reports indicate that plasma renin activity and plasma angiotensin II
concentrations are elevated in obesity, possibly as a consequence of increased sympathetic
outflow to the kidney.63,64 In obese hypertensive patients, pharmacologic blockade with
angiotensin- converting enzymes (ACEs) or angiotensin II receptor blockers ameliorate
hypertension and associated metabolic derangements, and reduce the incidence of type 2
diabetes.65 Additionally, adipose tissue expresses all components of the reninangiotensin
system (angiotensinogen, renin, ACE, angiotensin type 1 and type 2 receptors). Preliminary
evidence suggests that activation of an adipose reninangiotensin system is associated with high
blood pressure in a model of visceral obesity66,67 and in adipose tissue from obese hypertensive
patients.68
Pengaktifan reninangiotensin sistem boleh juga menyokong ke hipertensi terkait dengan
obesitas. pada hypertensive pasien obesitas, blokade pharmacologic dengan angiotensinmengubah enzim ( AS) atau angiotensin II sel yang peka rangsangan blockers memperbaiki
hipertensi dan berhubungan berkenaan dengan metabolism gangguan, dan mengurangi timbulnya
diabetes. Bukti persiapan menyatakan bahwa pengaktifan dari suatu adipose reninangiotensin
sistem dihubungkan dengan tekanan darah tinggi di pada suatu model obesitas mendalam dan di
dalam adipose jaringan/tisu dari pasien yang obesitas.

Impaired endothelial function

The vascular endothelium plays a major role in the regulation of vascular resistance.
Endothelium-derived nitric oxide bioactivation is an important determinant of vascular
relaxation. Vascular endothelial dysfunction is associated with a number of cardiovascular risk
factors, including obesity, insulin resistance, and hypertension.35,36 Reduced endotheliumdependent coronary and peripheral arterial vasodilation are more strongly correlated with waistto-hip ratio than with BMI. Visceral fat, quantified by abdominal computed tomography or
ultrasound is independently linked to impaired vasoreactivity. Weight loss improves endothelial
function.69

Endothelial berfungsi lemah

Endothelium yang vaskuler main suatu peran utama di dalam peraturan tentang pembalasan
vaskuler. Oksida berisi nitrat Endothelium-derived Bioactivation adalah suatu faktor penentu
yang penting dari relaksasi vaskuler. Endothelial vaskuler Kelainan fungsi tubuh dihubungkan
dengan suatu nomor;jumlah tentang faktor resiko cardiovasculer, mencakup kegendutan,
pembalasan hormon insulin, dan hypertension. Obesitas mendalam, yang terukur oleh
tomography dihitung abdominal atau ultrasound dengan bebas dihubungkan ke vasoreactivas
lemah. Kerugian Berat meningkatkan fungsi endothelial.
Adipokines
Adipose tissue is increasingly recognized as an endocrine organ with many secretory
products. Over 50 different adipocyte- derived substances have been identified, and many of
these substances have been implicated in blood pressure control. To date, leptin has been the
most thoroughly studied.
Adipokines
Jaringan Adipose terus meningkat dikenal sebagai suatu organ endocrine. (Di) atas 50 berbeda
adipocyte- unsur yang diperoleh telah dikenali, dan banyak dari unsur ini telah mencakup
pengendalian tekanan darah.
Leptin is a 167 amino acid peptide that promotes weight loss by reducing appetite and by
increasing energy expenditure through sympathetic stimulation to thermogenic tissue.70 The
effects of leptin are primarily mediated by receptors located in the central nervous system. The
absence of leptin or a mutation in the leptin receptor induces hyperphagia and obesity in both
rodents and humans. Circulating levels of leptin parallel fat cell mass. Blood pressure and leptin
are modestly correlated in normotensive and hypertensive individuals after adjustment for fat
mass.71 Two prospective studies have reported that plasma leptin concentration independently
predicts the onset of hypertension.72,73 Although these associations do not necessarily indicate
causality, chronic systemic and intracerebral administration of leptin increases blood pressure in
rats.71 Transgenic mice overexpressing leptin develop hypertension, despite weight loss, and
conversely, blood pressure is not increased in the obese, leptin deficient ob/ob mouse71 or in
obese, leptin deficient humans.74

Leptin adalah suatu 167 amino peptide asam yang mempromosikan kerugian berat/beban
dengan mengurangi selera dan dengan terus meningkatnya pengeluaran energy melalui
rangsangan simpatik ke tissue. Ketidakhadiran leptin atau suatu mutasi di dalam sel leptin yang
peka rangsangan mempengaruhi hyperphagia dan obesitas pada kedua binatang pengerat dan
manusia. Dua calon studi sudah melaporkan konsentrasi plasma leptin itu yang dengan bebas
memprediksi serangan hypertensi. Walaupun asosiasi ini lakukan tidak harus menandai adanya
hubungan sebab akibat, systemic kronis dan intracerebral administrasi leptin meningkatkan
tekanan darah di dalam tikus itu. Tikus-Tikus Transgenic yang overexpressing leptin
kembangkan hipertensi, di samping kerugian berat/beban, dan dan sebaliknya, tekanan darah
tidak meningkat pada tikus obesitas, leptin manusia tak mencukupi.
Increased sympathetic outflow is a putative mechanism by which leptin may increase arterial
pressure. Leptin activates the sympathetic nervous system both by centrally mediated effects on
the hypothalamus and by local peripheral actions.75 In humans, results of studies of the
association of plasma leptin with skeletal muscle nerve activity (measured by peroneal nerve
microneurography) are conflicting. High circulating levels of leptin reportedly account for much
of the increase in renal sympathetic tone observed in obese human subjects.76 Because obesity is
almost invariably associated with leptin resistance, it has been postulated that the resistance to
the weight-reducing effect of leptin is selective, and does not extend to leptins potential
sympathetic and cardiovascular actions. Although acute infusion of leptin produces natriuresis in
normotensive rats, the natriuretic effect is attenuated in hypertensive and obese Zucker rats,
possibly as a consequence of leptin resistance.77
Leptin mengaktipkan sistem nerves yang simpatik baik melalui hypothalamus dan oleh
sekeliling local actions. pada manusia, hasil studi asosiasi plasma leptin dengan aktivitas syaraf
otot yang diukur dengan peroneal syaraf microneurography adalah berlawanan. Walaupun
penuangan leptin yang akut menghasilkan natriuresis pada normotensive, efek yang natriuretic
disusutkan hypertensive dan obesitas, mungkin sebagai konsekwensi tentang leptin pembalasan.
Preliminary evidence suggest that other adipocyte-derived peptides may also affect arterial
pressure. Circulating adiponectin levels are decreased in obesity-induced insulin resistance,70
and some studies suggest that adiponectin is protective against hypertension through an
endothelial-dependent mechanism.78 A positive relationship between resistin and hypertension
has recently been described.
beberapa studi menyatakan bahwa adiponectin bersifat melindungi melawan terhadap
hipertensi melalui/sampai suatu endothelial-dependent mechanism. Suatu hubungan hal positif
antar[a] resistin dan hipertensi telah baru-baru ini uraikan.
Insulin resistance
Insulin resistance may be a link between obesity and hypertension. Obesity is associated with
resistance to insulin-stimulated glucose uptake and hyperinsulinemia, and weight loss increases
insulin sensitivity.37 Independent of obesity, centripetal distribution of body fat is associated
with insulin resistance and blood pressure. A metabolic consequence of insulin resistance is an
impaired capacity of postprandial hyperinsulinemia to suppress lipolysis, resulting in greater free

fatty acid release, particularly in upper body/visceral obesity compared with the nonobese or
lower body obesity. Release of free fatty acids due to excess adipose tissue lipolysis in upper
body obesity contributes to the metabolic abnormalities and possibly to the vascular dysfunction
associate with upper body obesity.30 Experimental evidence suggests that systemic free fatty
acids, derived primarily from subcutaneous adipose tissue, may mediate hypertensive
mechanisms attributed to insulin resistance. However, many of these studies have been
conducted at supraphysiologic concentrations of free fatty acids, and consequently these
observations should be considered tentative.

Pembalasan Hormon insulin

Obesitas dihubungkan dengan pembalasan ke insulin-stimulated pengambilan glukosa dan
hyperinsulinemia, dan peningkatan kerugian berat/beban hormon insulin sensitivity. Tidak terikat
pada kegendutan, distribusi bergerak menuju pusat tentang badan yang gemuk dihubungkan
dengan hormon insulin pembalasan dan tekanan darah. Suatu konsekwensi pembalasan hormon
insulin berkenaan dengan metabolism adalah suatu kapasitas yang lemah setelah makan malam
hyperinsulinemia untuk menindas lipolysis, menghasilkan pelepasan/release zat asam yang
mengandung gemuk cuma-cuma lebih besar, Bagaimanapun, banyak dari studi ini telah
diselenggarakan pada konsentrasi supraphysiologic dari zat asam yang mengandung lemak, dan
sebagai konsekwensi pengamatan ini harus dipertimbangkan karena bersifat sementara.
Whether hypertension is causally related to insulin resistance and/or hyperinsulinemia
remains an unresolved issue. In several rodent models of experimental hypertension,
hypertension can be ameliorated or prevented by chemically diverse agents that increase insulin
sensitivity or have a primary lipidlowering effect (e.g., thiazolidinediones, metformin, clofibrate,
lovastatin).79 Putative mechanisms by which insulin resistance and/or hyperinsulinemia may
increase blood pressure include an antinatriuretic effect of insulin, increased sympathetic nervous
system activity, augmented responses to endogenous vasoconstrictors, altered vascular
membrane cation transport, impaired endothelium-dependent vasodilatation, and stimulation of
vascular smooth muscle growth by insulin.
Pada beberapa model binatang pengerattentang hipertensi yang bersifat percobaan, hipertensi
dapat diperbaiki atau dicegah secara kimiawi. Mekanisme yang bereputasi baik dengan mana
pembalasan hormon insulin dan hyperinsulinemia dapat meningkatkan tekanan darah meliputi
suatu efek hormon insulin antinatriuretic, meningkat simpatik aktivitas sistem nerves,
ditambahkan menjawab endogen vasoconstrictors, mengubah pengangkutan kation selaput
vaskuler, endothelium-dependent lemah vasodilatation, dan rangsangan tentang pertumbuhan
otot lembut vaskuler dengan hormon insulin.
Clinical Management
Lifestyle interventions for treatment of obesity include emphasis on nutrition, physical
activity, and behavior modification. The increasing prevalence of obesity, including childhood
obesity, has stimulated interest in developing and evaluating strategies for obesity prevention.
Effective strategies for preventing and controlling overweight and obesity over a short term have

been implemented in worksite settings. These interventions have combined instruction in

healthier eating with a structured approach to increasing physical activity in the workplace.80
Interventions for preventing obesity in children have recently been reviewed.81 Nineteen of 22
studies included in the review were school/preschool-based interventions. The majority of
studies were of short term. Nearly all studies resulted in some improvement in diet and physical
activity. Some studies that focused on either diet or physical activity alone, but not in
combination, had a small but positive impact on BMI.

Manajemen Klinis
Obesitas, mencakup obesitas masa kanak-kanak, telah merangsang minat akan
mengembangkan dan mengevaluasi strategi untuk pencegahan obesitas. Strategi efektif untuk
mencegah dan mengendalikan kelebihan berat dan obesitas suatu jangka pendek mempunyai
worksite yang ditentukan. Hampir semua studi muncul dalam beberapa peningkatan diet dan
aktivitas fisik. Beberapa studi yang yang dipusatkan baik diet maupun aktivitas phisik sendiri,
tetapi bukan kombinasi, yang kecil tapi berdampak positif pada BMI.
In two small towns in France, a comprehensive and innovative community-based program to
prevent obesity in schoolchildren involved the mayor, teachers, health-care providers, food
providers, sports associations, the media, scientists, and various branches of town government.82
The towns built sporting facilities, playgrounds, mapped out walking itineraries, and hired sports
instructors. Families were offered cooking workshops and families at risk were offered
individual counseling. Between 2000 and 2005, the prevalence of overweight in children had
fallen to 8.8%, whereas it had risen to 17.8% in neighboring comparison towns. This total
community approach is now being extended to 200 towns in Europe under the name EPODE
(Ensemble, prevenons lobesite des enfants (Together, lets prevent obesity in children)).83
Pada dua kota kecil di Perancis, terdapat program inovatif dan menyeluruh untuk mencegah
obesitas pada anak-anak sekolah yang melibatkan walikota, para guru, penyedia pelayanan
kesehatan, penyedia makanan, asosiasi olahraga, media, ilmuwan, dan berbagai cabang kota.
Kota membangun fasilitas olahraga, tempat bermain, merencanakan rencana perjalanan, dan
menyewa sports instruktur. Keluarga-Keluarga telah ditawarkan memasak tempat kerja dan
keluarga-keluarga berhadapan dengan resiko dan menasehatinya.
Several different diets have been advocated for the treatment of obesity (e.g., very-low-calorie
diets, balanced-deficit diets, low-fat diets, low-carbohydrate diets, high-protein diets), and
weight loss occurs with each of them.84 A number of behavioral strategies, administered either
individually or groups, may assist with adherence. As recently reviewed,83 behavioral packages
may include food diaries and activity records, control of stimuli that activate eating, slower rate
of eating, goal setting, behavioral contracting and reinforcement, nutrition education, meal
planning, social support, cognitive restructuring and problem solving. Incorporation of increased
physical activity (e.g., activity that expends ~2,500 kcal/week) in the regimen increases the

likelihood of maintaining weight loss. Nevertheless, the recidivism rate is high. Approximately
90% of people who lose weight by dieting regain it within 35 years.85
Beberapa diet berbeda telah didukung untuk perawatan tentang kegendutan ( e.g., very-lowcalorie diet, balanced-deficit diet, low-fat diet, low-carbohydrate diet, high-protein diet), dan
kerugian berat/beban terjadi dengan masing-masing them. [Adalah] suatu nomor;jumlah tentang
tingkah laku strategi, mengatur yang manapun secara individu atau kelompok, boleh membantu
dengan kesetiaan. penentuan sasaran, penguatan dan terikat kontrak tingkah laku, pendidikan
ilmu gizi, perencanaan makanan, pen;dukungan sosial, restrukturisasi teori dan pemecahan
masalah. Persatuan/Perseroan tentang aktivitas phisik ditingkatkan ( e.g., aktivitas yang
membelanjakan ~ 2,500 kcal/week) di (dalam) cara hidup meningkat/kan kemungkinan
memelihara kerugian berat/beban. Meskipun demikian, tingkat tarip residivisme adalah tinggi.
Kira-Kira 90% dari orang yang menurunkan berat dengan diet memperoleh kembali ia/nya di
dalam 35 years.
For patients with BMI >27 kg/m2 who do not respond to a trial of diet, exercise, and behavior
therapy, pharmacotherapy can be tried. Two medications are currently available in the United
States for the treatment of obesity: (i) orlistatan inhibitor of pancreatic lipase that reduces
intestinal digestion of fat and (ii) sibutraminea serotoninnorepinephrine reuptake inhibitor.84
Orlistat is associated with steatorrhea, and sibutramine may actually increase blood pressure and
blunt the decrease associated with weight loss. In adolescents, metformin has recently been
shown to cause a small but statistically significant decrease in BMI when added to a lifestyle
intervention program.86 Bariatric procedures are being performed with increasing frequency for
patients with BMI >40 kg/m2 or BMI >35 kg/m2 with associated comorbidities.87 In the short
term, blood pressure has been shown to decrease in response to orlistat and to bariatric
surgery.88,89 However, hypertension per se is generally not considered an indication for these
pharmacologic or surgical approaches.
Dua pengobatan sekarang ini tersedia Amerika Serikat untuk perawatan obesitas: ( i) orlistat
an penghambat lipase tentang pankreas yang mengurangi pencernaan berhubungan dengan
usus tentang obesitas dan ( ii) sibutraminea serotoninnorepinephrine pengambilan kembali
Inhibitor. Prosedur Bariatric sedang yang dilakukan dengan meningkatkan frekwensi untuk
pasien dengan BMI > 40 kg/m2 atau BMI > 35 kg/m2 dengan comorbidities. dihubungkan
Dalam jangka pendek, tekanan darah telah menunjukan pengurangan
Many predominantly short-term (6-week to 6-month duration) clinical trials document that
even moderate weight loss (510%) results in reduction of blood pressure and hypertension
incidence, and improvement in insulin sensitivity and vascular endothelial function.36,69
Reviews of randomized trials reported a diastolic reduction of 0.92 mm Hg and a systolic
reduction of 1 mm Hg/kg of weight loss.90 However, review of longer term trials, including
trials of bariatric surgery, suggests that the maximum effect of weight loss on blood pressure
occurs during and soon after weight loss and that this effect is attenuated in the long term.91
Banyak [yang] jangka pendek ( 6-week ke jangka waktu 6-bulan) dokumen percobaan/ klinis
yang genap kerugian berat/beban moderat ( 510%) menghasilkan pengurangan tekanan darah

dan timbulnya hipertensi , dan peningkatan pada kepekaan hormon insulin dan fungsi vaskuler
endothelial. Tinjauan ulang dari percobaan randomized yang dilaporkan suatu pengurangan
diastolie 0.92 Mm Hg dan pengurangan sistole 1 Mm Hg/kg berat menurun.
In addition to weight loss and other lifestyle modifications, many if not most obese,
hypertensive patients ultimately require treatment with one or more antihypertensive agents for
blood pressure control. There is little clinical trial data to indicate that any one class of agents is
superior to others. Most guidelines do not recognize obese patients as a special population, and
do not make specific recommendations for the pharmacologic treatment of hypertension
associated with obesity.
Sebagai tambahan terhadap berkurangnya berat dan modifikasi gaya hidup, banyak jika bukan
obesitas, pasien hipertensi akhirnya memerlukan perawatan dengan satu atau lebih
antihypertensive untuk mengendalikan tekanan darah. Kebanyakan petunjuk tidak mengenali
pasien obesitas sebagai populasi khusus, dan tidak membuat rekomendasi spesifik untuk
perawatan farmakologi hipertensi yang berhubungan dengan obesitas.
The general principles of pharmacotherapy for obese patients are not different from nonobese
patients, but there are a few caveats. The capacity of thiazide diuretics to lower blood pressure in
obese hypertensive patients is well established,92 and the adverse metabolic effects of diuretics
(insulin resistance, dyslipidemia, hypokalemia) are dose related. ACE inhibitors, and possibly
angiotensin II receptor blockers, increase insulin sensitivity and reduce diabetes risk.93,94 Some
consider ACE inhibitors to be the most appropriate medication for blood pressure control in
obese hypertensive patients.95,96 Although the recent DREAM (Diabetes Reduction Assessment
with Ramipril and Rosiglitazone Medication) study suggests that the reduction in diabetes risk
with ACE inhibition in patients with low cardiovascular risk was not as pronounced as expected,
that study did not target an obese hypertensive population.97 In the PROGRESS (Perindopril
Protection Against Recurrent Stroke Study) trial, compared to placebo, blood pressure lowering
with perindopril resulted in comparable risk reductions in vascular disease in normal weight,
overweight, and obese individuals with a history of stroke.98 The greatest benefit was observed
in those with higher BMIs, possibly because they had higher levels of cardiovascular risk at
baseline, including higher blood pressures. The antihypertensive potencies of lisinopril and
hydrochlorothiazide were reportedly similar in a study of 223 predominantly white, obese,
hypertensive patients.99 Several trials have documented the efficacy of the combination of
hydrochlorothiazide with either an ACE, an ARB, or the renin inhibitor aliskiren in obese
hypertensive patients.100
Prinsip pharmacotherapy yang umum untuk pasien obesitas tidaklah berbeda dari pasien yang
tidak obesitas, tetapi ada beberapa surat protes penegakan hukum. Beberapa mempertimbangkan
AS penghambat sebagai pengobatan yang paling sesuai untuk darah kendali tekanan di (dalam)
gemuk sekali hypertensive patients. pasien dengan resiko yang memiliki tingkat cardiovasculer
rendah bukanlah dilafalkan seperti yang diharapkan, studi itu tidak mentargetkan suatu
population orang obesitas dan hipertensi. mungkin sebab mereka mempunyai tingkat yang lebih
tinggi untuk resiko cardiovasculer, termasuk lebih tinggi tekanan darah.

-Blockers may more effectively decrease blood pressure in obese than in lean hypertensives,
perhaps because they decrease cardiac output and plasma renin activity, both of which are
increased in obese patients. However, -blockers may be associated with weight gain and have
negative effects on glucose metabolism.101 The use of -blockers as first line agents has been
questioned because their effect on stroke protection does not compare favorably with other
antihypertensive agents.100 Although calcium antagonists do not have adverse metabolic side
effects, and -blockers have been associated with improved insulin sensitivity and lipid
metabolism, there is no compelling reason to use these as first line agents in obesity-related
hypertension.
b- Blockers dapat lebih secara efektif mengurangi tekanan darah pada obesitas.
Bagaimanapun, b- blockers mungkin dihubungkan dengan kelebihan berat badan dan
mempunyai hal negatif yang mempengaruhi metabolisme glukosa. b- blockers telah
dihubungkan dengan meningkatnya kepekaan hormon insulin dan metabolism lipid, tidak ada
alasan yang memaksa untuk menggunakan ini sebagai yang utama pada hipertensi terkait dengan
obesitas
In the final analysis, similar to treatment of all hypertensive patients, combinations of agents
with complimentary mechanisms may be required to achieve blood pressure goals. Selection of
drugs should be individualized, taking into account the severity of hypertension, other CVD risk
factors, comorbid conditions, and practical considerations related to cost, side effects, and
frequency of dosing.
Pada analisa yang terakhir, serupa dengan perawatan dari semua pasien hypertensi, Pemilihan
obat harus dibedakan dari yang lain. mengambil factor resiko CVD , kondisi comorbid, dan
pertimbangan praktis berhubungan dengan biaya, efek samping, dan frekwensi dosis.
Summary
Obesity-related hypertension is a multifactorial phenotype determined by the interaction of genes and
environments. However, currently identified genomic factors account for only a small percent of the
heritable risk of this phenotype. The association of hypertension with obesity is primarily related to
visceral obesity, which in turn is associated with insulin resistance and dyslipidemia. Lifestyle and
pharmacologic approaches for treating obesity-related hypertension should address overall CVD risk, not
simply hypertension. More work is required to identify culturally sensitive strategies for obesity
prevention and their impact not only on body weight, but also on blood pressure, the metabolic
phenotypes associated with obesity, and subsequent CVD. Although several mechanisms have been
identified that may account for elevated arterial pressure, currently, there is no compelling evidence to
indicate that any one class of antihypertensive agents is particularly advantageous for the treatment of
obesity- related hypertension.

Ringkasan
Hipertensi terkait dengan obesitas adalah suatu multi faktor fenotip yang ditentukan oleh
interaksi gen dan lingkungan. Bagaimanapun, faktor genomic sekarang ini dikenali meliputi
hanya suatu persen yang kecil resikonya dan turun temurun. Asosiasi hipertensi dengan obesitas
terutama semata obesitas mendalam, yang mana pada gilirannya dihubungkan dengan
pembalasan hormon insulin dan dyslipidemia. Gaya hidup dan pendekatan farmakologi untuk
hipertensi terkait dengan obesitas perlu menunjuk keseluruhan resiko CVD, tidak hanya

hipertensi. Walaupun beberapa mekanisme telah dikenali itu misalnya seperti meningkatnya
tekanan urat nadi , sekarang ini, tidak ada yang memaksa bukti untuk menunjukkan bahwa tiap
orang kelas antihypertensive yang menguntungkan untuk perawatan obesitas- hipertensi yang
terkait.