reninanjiyotensinaldosteron

The renin-angiotensin-aldosterone system (RAAS) is a hormonal cascade that regulates blood pressure, extracellular fluid volume, and electrolyte balance. It involves renin, angiotensinogen, angiotensin I and II, aldosterone, and the enzymes renin, angiotensin-converting enzyme (ACE), and ACE2, as well as angiotensin receptors. The system is activated by signals such as reduced renal perfusion, decreased sodium chloride delivery to the macula densa, and sympathetic nervous activity.

Renin, released from juxtaglomerular cells in the kidney, cleaves angiotensinogen produced by the liver to form angiotensin I. ACE, mainly in the lungs and endothelium, converts angiotensin I to angiotensin II, a potent vasoconstrictor. Angiotensin II stimulates aldosterone secretion from the adrenal cortex, promotes sodium reabsorption and potassium excretion in the distal nephron, increases water reabsorption, and enhances thirst and antidiuretic hormone release. These actions raise blood pressure and blood volume. Angiotensin II also acts on various tissues to provoke inflammatory and fibrotic responses in some pathological states.

Regulation includes negative feedback of renin release by rising blood pressure and renal perfusion. A counter-regulatory axis involves ACE2 converting angiotensin II to angiotensin-(1-7), which can oppose many of the vasoconstrictive and pro-proliferative effects of Ang II.

Clinical relevance and therapy: overactivation contributes to hypertension, heart failure, and chronic kidney disease. Pharmacologic blockade includes ACE inhibitors, angiotensin II receptor blockers (ARBs), direct renin inhibitors, and mineralocorticoid receptor antagonists. Side effects vary by class, including cough and angioedema with ACE inhibitors and hyperkalemia with MR antagonists.