Blood Pressure Regulation

Flow = pressure gradient / resistance

CO = MAP / TPR

Therefore MAP=CO x TPR = HR x SV x TPR

TPR is the total peripheral resistance: this is the combined resistance of all blood vessels (remember
the importance of vasodilation and vasoconstriction)

Arterial Pressure

Systolic Pressure (120 mmHg)

Systolic Pressure (120 mmHg) occurs with ventricular contraction

Diastolic Pressure (80 mmHg)

Diastolic Pressure (80 mmHg) occurs with ventricular refilling

Regulation of MAP

 Short-term regulation – seconds to minutes (baroreceptor reflex)

Involves heart and blood vessels →regulate blood vessel diameter, heart rate and
contractility

Primarily neuronal control

 Long-term regulation – minutes to days

Regulation of blood volume

Involves kidneys

Primarily hormonal control

Short-Term Regulation Blood Pressure

>>Rising blood pressure

1. Stretching of arterial walls

2. Stimulation of baroreceptors in carotid sinus, aortic arch, and other large arteries of the neck
and thorax

Effect of Baroreceptors

• Increased impulses to brain from baroreceptors

• Increased parasympathetic activity and decreased sympathetic activity

 Effect of Increased Parasympathetic and Decreased Sympathetic Activity on Heart
and Blood Pressure:

• Increased activity of vagus (parasympathetic) nerve • Decreased activity of

sympathetic cardiac nerves

• Reduction of heart rate

• Lower cardiac output

• Lower blood pressure

• Reduction of heart rate and increase in arterial diameter

• Lower blood pressure

3. Increased impulses to the brain

>> Falling Blood Pressure:

1. Falling blood pressure

2. Baroreceptors inhibited
3. Decreased impulses to the brain
4. Decreased parasympathetic activity, increased sympathetic activity

> Three effects:

o Heart: increased heart rate and increased contractility

o Vessels: increased vasoconstriction
o Adrenal gland: release of epinephrine and norepinephrine which enhance heart
rate, contractility, and vasoconstriction

Effect of Increased Sympathetic Activity on

1. Heart and Blood Pressure

• Increased activity of sympathetic cardiac nerves
• Decreased activity of vagus (parasympathetic) nerve
• Increased heart rate and contractility
• Higher cardiac output
• Increased blood pressure
2. Vasomotor Fibers

Effect of Increased Sympathetic Activity on Arteries and Blood Pressure:

• Increased activity of vasomotor fibers (sympathetic nerve fibers)

• Constriction of vascular smooth muscle
• Decreased arterial diameter
• Increased blood pressure
3. Adrenal Gland and Blood Pressure
• Increased sympathetic impulses to adrenal glands
 • Release of epinephrine and norepinephrine to bloodstream
• Hormones increase heart rate, contractility and vasoconstriction. Effect is slower-
acting and more prolonged than nervous system control.
• Increased blood pressure
5. Increased blood pressure

Penjelasan tambahan tentang baroreceptor 

Baroreceptors
 Specialised nerve endings
Respond to stretch of vessel wall; indirect response to changes in BP
 Location
Carotid sinus
Aortic Arch
 Type
A fibres (myelinated)
Low pressure (30-90 mmHg)
Important at rest
C fibres (unmyelinated)

High pressure (70-140 mmHg)

Increasingly active at higher pressures

Central Control of CVS

 Involves integrated responses from:
Medulla, hypothalamus, cerebral cortex, cerebellum
 Baroreceptor input to NTS in medulla (nucleus tractus solitarius)
 Output to:
o Parasympathetic NS (vagus) via nucleus ambiguus
Cardiac control (limits HR)
o Sympathetic NS via rostral ventrolateral medulla
Cardiac and blood vessel control (↑ed contractile strength/tone)
 o Hypothalamus & amygdala in cerebellum
Overriding output during stress to raise BP

Extra Inputs to CVS Control

 Atrial stretch receptors
o Myelinated vagal afferents sensitive to blood volume
o Located at junction of “great veins” and atria
o Influences endocrine regulation of blood volume via:
Hypothalamic ADH → renal water retention
Renin-Angiotensin-aldosterone system (RAS) → renal salt & water retention
Atrial Natriuretic Peptide → renal salt & water excretion
 Bainbridge reflex
o Vena cava stretch receptors → neural mediated ↑HR
o Avoids venous congestion
Long-Term Regulation of Low BP

• Long-term regulation of blood pressure is primarily accomplished by altering blood volume.

• The loss of blood through hemorrhage, accident, or donating a pint of blood will lower blood
pressure and trigger processes to restore blood volume and therefore blood pressure back to
normal.

• Long-term regulatory processes promote the conservation of body fluids via renal mechanisms and
stimulate intake of water to normalize blood volume and blood pressures.
Renin-angiotensin-aldosterone

system Most important hormonal system involved in regulating Na+

Aldosterone Mechanism

• Long-Term Regulation:

Aldosterone promotes increased reabsorption of sodium from the kidney tubules.

Aldosterone stimulates the cells of the distal convoluted tubule to increase the active transport of
sodium ions out of the tubule into the interstitial fluid, accelerating sodium reabsorption.

As sodium moves into the bloodstream, water follows. The reabsorbed water increases the blood
volume and therefore the blood pressure.

Osmolarity on BP

>Short-Term Effect of Osmolarity on BP

A short-term effect of increased osmolarity is the excitation of the thirst center in the hypothalamus.
The thirst center stimulates the individual to drink more water and thus rehydrate the blood and
extracellular fluid, restoring blood volume and therefore blood pressure.

>Long-Term Effect of Osmolarity on BP

 As increased osmolarity is detected there is both a short and long-term effect. For the long-term
effect, the hypothalamus sends a signal to the posterior pituitary to release antidiuretic hormone
(ADH).

ADH promotes the reabsorption of water from the kidney by stimulating an increase in the number
of water channels in the distal convoluted tubules and collecting tubules (ducts). These channels aid
in the movement of water back into the capillaries, decreasing the osmolarity of the blood volume
and therefore blood pressure.

Case! Hypertension

 Primarily arises via ↑ed peripheral flow resistance

 5% of cases
o disturbance of normal physiological function disturbance of normal physiological
function
o e.g. renal diseases, adrenal diseases e.g. renal diseases, adrenal diseases (associated
with salt & water retention, & (associated with salt & water retention, & ↑ blood
vol.) blood vol.)
 95% of cases
“essential hypertension ssential hypertension”
Mostly via aspects that affect arteriolar smooth muscle
Cumulative effect of genetic, lifestyle & environmental factors