reninangiotensin

Renin-angiotensin system (RAS) is a hormone cascade that regulates blood pressure, fluid and electrolyte balance, and vascular tone. It begins with renin, an enzyme produced by juxtaglomerular cells in the kidney in response to reduced renal perfusion, decreased sodium chloride delivery to the distal tubule, or sympathetic stimulation. Renin cleaves circulating angiotensinogen, produced by the liver, to form angiotensin I.

Angiotensin I is converted to angiotensin II primarily by angiotensin-converting enzyme (ACE) on vascular endothelium. Angiotensin II is a potent vasoconstrictor and stimulates aldosterone secretion from the adrenal cortex, leading to sodium and water reabsorption in the kidneys. The system is tightly regulated by feedback: low blood pressure or low sodium chloride at the macula densa promotes renin release, while high blood pressure or increased NaCl delivery inhibits it.

Angiotensin II acts mainly through angiotensin receptors, particularly the type 1 receptor (AT1R) and the type 2 receptor (AT2R). AT1R mediates vasoconstriction, aldosterone secretion, thirst, and antidiuretic hormone release, contributing to increased blood pressure and volume. AT2R can oppose some AT1R effects and may promote vasodilation and tissue repair in some contexts.

Clinical relevance includes the association of-RAS overactivity with hypertension, heart failure, and chronic kidney disease. Therapeutic strategies targeting the renin-angiotensin system include ACE inhibitors, which block the conversion of angiotensin I to II; angiotensin II receptor blockers (ARBs), which prevent AT1R activation; and direct renin inhibitors that reduce renin activity. Non-ACE pathways can also generate angiotensin II, underscoring residual activity in some treatments.