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Diuretics and renal hormones

CONTENTS

Physiologic hormones affecting the kidney

Diuretics

DIURETICS AND RENAL HORMONES

Sultan Chaudhry (http://www.pathophys.org/author/sultan/)

Physiologic hormones aecting the kidney

Hormone Trigger and pathway Site of action in Net eect

the nephron
(see figure)

Angiotensin II Synthesized in response to Aerent and 1. Aerent and eerent

(Ang II) hypotension. (See AKI
(http://www.pathophys.org/aki/)
and CKD
(http://www.pathophys.org/ckd/)
chapters for details of Ang II
production pathway)
eerent arteriole (higher degree) arteriolar
constriction leading to a
rise in GFR.
2. Compensatory sodium
absorption occurs in the
proximal as well as the
distal nephron to
maintain fluid balance
(via water osmosis
following sodium).

Atrial Released in response to Aerent and 1. Aerent arteriolar dilation

natriuretic increased atrial pressure. eerent arteriole, and eerent arteriolar
peptide (ANP) distal convoluted constriction leading to an
tubule (DCT). overall increase in GFR
and increase in sodium
filtration.
2. At the DCT, it inhibits
sodium uptake to ensure
 volume loss.

Vitamin D3 Hypocalcemia DCT Increased calcium uptake.

(calcitriol)

Parathyroid Hypocalcemia and Ascending limb Increased calcium uptake.

hormone hyperphosphatemia,and/or low of loop of Henle
(PTH) vitamin D levels. (LoH) and DCT

Aldosterone Hypovolemia and hypotension Collecting duct Increased sodium uptake

(via Ang II), and/or hyperkalemia (CD) and potassium excretion
into the urine. Causes net
fluid retention.

Antidiuretic Hypovolemia and hypotension CD Increases free water uptake

hormone (via Ang II), increased plasma from the collecting duct.
(ADH) osmolality

(http://www.pathophys.org/diuretics/mpr-nephron/)
The nephron showing reabsorption, hormone action, and diuretic action.

Diuretics

Diuretic type (example) Site of Mechanism (see figure)

action

Carbonic anhydrase Proximal Acetazolamide is a carbonic anhydrase (CA) inhibitor. CA

inhibitor (acetazolamide) convoluted is an enzyme involved in the breakdown of carbonic acid
tubule (PCT) in the following reaction:
H2O + CO2 CA H2CO3 HCO3 + H+
Under physiologic conditions, filtered bicarbonate
combines with the hydrogen ions to generate carbonic
acid, which is acted on by CA to make CO2 and H2O. As
the CO2 diuses into the tubular cells, more bicarbonate is
absorbed from the serum. In the presence of
acetazolamide, CA is inhibited, allowing for the H2CO3 to
build up in the tubules and hence urinary bicarbonate
wasting (H+ alternatively is reabsorbed via a dierent
pathway). This leads to a decreased ability to reabsorb
Na+ in exchange for H+, leading to mild diuresis.

Osmotic (mannitol) PCT Mannitol is filtered through the glomerulus but cannot be
reabsorbed. This increases the osmolality of the filtrate
and water is retained in the tubules to ensure urine
osmolality.
 Loop (furosemide) Loop of Blocks the sodium potassium chloride pump (NKCC) in
Henle the thick ascending limb of loop of Henle. This allows for
more sodium and subsequently fluid loss from the
nephrons.

Thiazide DCT Thiazide diuretics block the activity of sodium chloride

(hydrochlorothiazide) channels (Na-Cl) in the DCT allowing more sodium and
water loss.

Potassium Sparing CD Aldosterone acts on the cells of the collecting ducts and
1. Aldosterone induces expression of Na/K exchangers and ENaC. This
Antagonists allows for the exchange of sodium for potassium (Na
(spironolactone) enters the tubular cells and K is lost in the urine).
2. Epithelial sodium Aldosterone antagonists competitively inhibit the action of
channel (ENaC) aldosterone on the principal cells and therefore decrease
blocker (amiloride the expression of the exchanger. With the lack of sodium
and triamterene) uptake from the nephrons and loss in the urine, diuresis
also takes place.
Aldosterone also controls expression of ENaC channels in
the distal tubules to absorb sodium. Inhibition of the ENaC
decreases Na uptake and K loss from the tubular cells.
Loss of Na in the urine leads to mild diuresis.

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