angiotenzin

Angiotenzin is a peptide hormone central to the renin–angiotensin system, a hormonal cascade that regulates blood pressure, fluid balance, and electrolyte homeostasis. It is produced in precursor form as angiotensinogen by the liver and released into the circulation. Renin, an enzyme from the kidneys, cleaves angiotensinogen to angiotensin I, which is then converted to the active peptide angiotensin II by angiotensin-converting enzyme (ACE), primarily in the lungs and vascular endothelium. Additional pathways generate other angiotensin peptides, such as angiotensin III and angiotensin-(1–7), each with distinct activities.

Angiotensin II is the main effector peptide and acts through two receptor types, AT1 and AT2. Activation of AT1 receptors causes vasoconstriction, stimulates aldosterone secretion from the adrenal cortex, promotes sodium and water reabsorption in the kidneys, increases antidiuretic hormone release, and can contribute to inflammation and fibrosis. Angiotensin II also raises blood pressure and participates in pathologies including hypertension, heart failure, and chronic kidney disease.

Counter-regulatory pathways include ACE2, which converts angiotensin II to angiotensin-(1–7), a peptide that opposes many of angiotensin II’s actions by promoting vasodilation and anti-proliferative effects through the Mas receptor. The balance between the vasoconstrictive arm and this counter-regulatory arm influences vascular tone and organ protection.

Clinical relevance and therapy: Inhibiting the renin–angiotensin system is a major treatment strategy for hypertension, heart failure, and chronic kidney disease. ACE inhibitors (for example, enalapril, lisinopril) block the formation of angiotensin II; ARBs (losartan, valsartan) block AT1 receptors; direct renin inhibitors (aliskiren) reduce renin activity. Side effects may include cough, hyperkalemia, and, rarely, angioedema.