Abstract
Renin is an aspartyl peptidase that is synthesized, stored, and released from juxtaglomerular (JG) granular cells in the lamina media of the afferent arteriole. Each afferent arteriole contains 5–20 JG cells. Renin catalyzes the cleavage of angiotensin I (ANG I) from renin substrate; angiotensin I is further converted to the physiologically active form angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II (ANG II) is an important vasoconstrictor, and it promotes release of aldosterone from the adrenal gland. Thus, the renin-angiotensin-aldosterone system is important in the regulation of salt and water homeostasis and blood pressure. In keeping with its complex homeostatic roles, the regulation of renin secretion is under the control of a number of systemic factors. Release is stimulated by decreases in arterial pressure, increases in sympathetic nervous activity, and by a decrease in the tubular NaCl concentration at the macula densa (MD).
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© 2003 Humana Press Inc., Totowa, NJ
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Jensen, B.L., Friis, U.G., Skøtt, O. (2003). In Vitro Studies on Renin Release. In: Goligorsky, M.S. (eds) Renal Disease. Methods in Molecular Medicine™, vol 86. Humana Press. https://doi.org/10.1385/1-59259-392-5:341
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DOI: https://doi.org/10.1385/1-59259-392-5:341
Publisher Name: Humana Press
Print ISBN: 978-1-58829-134-9
Online ISBN: 978-1-59259-392-7
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