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Section on Pharmacology, Laboratory of Clinical Science, National Institute of Mental Health Bethesda, Maryland 20892
Correspondence: Address requests for reprints to: J. M. Saavedra, M.D., Section on Pharmacology, Laboratory of Clinical Science, National Institute of Mental Health, 9000 Rockville Pike, Building 10, Room 2D-45, Bethesda, Maryland 20892.
Abstract
I. Introduction: Angiotensin(ANG II) was discovered about 50 yr ago (1, 2), and a complete peripheral system for the formation and metabolism of ANG II was soon characterized. It was named the renin-angiotensin system, based on the rate-limiting enzyme, renin, and the active principle, ANG II (3). In the classical peripheral RAS system, a precursor molecule, angiotensinogen (AOGEN), originates in the liver and is cleaved to the essentially inactive decapeptide angiotensin I (ANG I) by an aspartyl protease, renin, synthesized and released to the circulation mainly by the juxtaglomerular cells of the kidney. ANG I is converted to ANG II, the effector peptide of this system, by the angiotensin-converting enzyme (ACE) (4). Circulating ANG II acts on high affinity ANG II receptors located in the vascular smooth muscle, zona glomerulosa of the adrenal gland, and kidney to produce vasoconstriction, aldosterone release, and sodium retention, respectively. Thus, the peripheral RAS is a hormonal system with important functions in the regulation of blood pressure and fluid homeostasis.
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