Angiotensin

Angiotensin refers to a group of peptide hormones that regulate blood pressure, fluid balance, and electrolyte homeostasis as part of the renin-angiotensin system (RAAS). The primary precursor is angiotensinogen, a protein produced mainly by the liver and circulating in plasma.

In the RAAS cascade, kidney-derived renin cleaves angiotensinogen to form angiotensin I, a decapeptide. Angiotensin-converting enzyme (ACE), largely in the lungs, then converts angiotensin I to angiotensin II, an octapeptide. Angiotensin II exerts its major effects via the AT1 receptor: vasoconstriction, stimulation of aldosterone release from the adrenal cortex (increasing sodium and water reabsorption), promotion of antidiuretic hormone release, and enhanced sympathetic activity. It also contributes to vascular remodeling and may promote inflammation and fibrosis. Angiotensin II can also interact with AT2 receptors, which can counterbalance some actions in certain contexts.

The RAAS involves other angiotensin peptides as well, including angiotensin III and angiotensin IV, with overlapping roles in regulation. Additionally, ACE2 can convert angiotensin II to angiotensin-(1-7), which generally opposes angiotensin II effects by promoting vasodilation via the MAS receptor. Angiotensin I and II differ in size, and angiotensin II is the principal effector peptide in blood pressure regulation.

Clinical significance centers on dysregulation of the RAAS in hypertension, heart failure, and chronic kidney disease. Therapeutic approaches include ACE inhibitors (for example, captopril, enalapril), angiotensin II receptor blockers (ARBs, such as losartan, valsartan), and renin inhibitors (e.g., aliskiren). Side effects of ACE inhibitors can include cough and, rarely, angioedema due to bradykinin accumulation.