Regulation of Kidney Function
சிறுநீரகச் செயல்பாட்டின் ஒழுங்குமுறை
ADH and the renin-angiotensin system both raise blood pressure and save water; ANF does the opposite. If an option has ANF 'released when blood pressure falls', it is wrong.
The idea
The functioning of the kidneys is efficiently monitored and regulated by hormonal feedback mechanisms involving the hypothalamus, the JGA and to a certain extent the heart. Osmoreceptors in the body are activated by changes in blood volume, body fluid volume and ionic concentration. An excessive loss of fluid from the body activates these receptors, which stimulate the hypothalamus to release antidiuretic hormone (ADH) or vasopressin from the neurohypophysis. ADH facilitates water reabsorption from the latter parts of the tubule, thereby preventing diuresis; an increase in body fluid volume switches off the osmoreceptors and suppresses ADH release. ADH can also affect kidney function by its constrictory effects on blood vessels, causing an increase in blood pressure, which may increase the glomerular blood flow and thereby GFR. A fall in glomerular blood flow, glomerular blood pressure or GFR activates the JG cells to release renin, which converts angiotensinogen in blood to angiotensin I and further to angiotensin II. Angiotensin II, a powerful vasoconstrictor, increases the glomerular blood pressure and thereby GFR; it also activates the adrenal cortex to release aldosterone, which causes reabsorption of Na+ and water from the distal parts of the tubule, again increasing blood pressure and GFR. This is the renin-angiotensin mechanism. An increase in blood flow to the atria of the heart causes release of atrial natriuretic factor (ANF), which causes vasodilation and thereby decreases blood pressure; the ANF mechanism acts as a check on the renin-angiotensin mechanism.
Why it matters
Water intake and loss change all day; hormones let the kidney save water and raise pressure when the body is short, and dump salt and water when there is excess.
NEET lens
Sequence questions: fall in GFR → renin from JG cells → angiotensinogen → angiotensin I → angiotensin II → vasoconstriction (↑BP, ↑GFR) + aldosterone → Na+ and water reabsorption from distal tubule. ADH prevents diuresis; excessive fluid loss switches ON osmoreceptors. ANF: released on increased atrial blood flow, causes vasodilation, lowers BP — so a decrease in BP will NOT cause ANF release.
Clinical significance
Defective ADH release or action causes diabetes insipidus — large volumes of dilute urine and dehydration. Common blood-pressure medicines (ACE inhibitors) work by blocking the formation of angiotensin II.
Introduction
The kidney's output is controlled by hormones from the hypothalamus (ADH), the JGA (renin-angiotensin-aldosterone) and the heart (ANF).
Core concept
ADH (vasopressin): excess fluid loss → osmoreceptors activated → hypothalamus → ADH released from neurohypophysis → water reabsorption from latter parts of tubule → prevents diuresis; ↑ body fluid volume switches osmoreceptors off. ADH also constricts blood vessels → ↑BP → may ↑GFR. Renin-angiotensin: ↓ glomerular blood flow/pressure/GFR → JG cells release renin → angiotensinogen → angiotensin I → angiotensin II (powerful vasoconstrictor → ↑glomerular BP and GFR) → adrenal cortex releases aldosterone → Na+ and water reabsorption from distal tubule → ↑BP and GFR. ANF: ↑ blood flow to atria → ANF → vasodilation → ↓BP; checks the renin-angiotensin mechanism.
Go deeper
Order for the 2026-type question: fall in GFR (III) → renin converts angiotensinogen to angiotensin I and then II (V) → vasoconstriction by angiotensin II and release of aldosterone (IV) → reabsorption of Na+ and water from distal tubule (II) → increase in BP and GFR (I).
From Class 10
Your body keeps blood pressure and water balance steady using hormones. This concept shows the exact chain the kidney uses.