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Mutations that alter renal salt handling. A diagram of a nephron is shown, and major mediators of renal salt reabsorption are shown. These include Na+/H+ exchange in the proximal tubule, Na+-K+-2Cl− cotransport in the thick ascending limb of Henle, Na-Cl cotransport in the distal convoluted tubule, and electrogenic Na+ reabsorption via the epithelial sodium channel (ENaC). The role of the renin-angiotensin system in the regulation of salt homeostasis is indicated. Renin, secreted by cells of the juxtaglomerular apparatus, cleaves angiotensinogen to angiotensin I, which is further processed by angiotensinconverting enzyme (ACE) to the active hormone angiotensin II. Angiotensin II binds to specific receptors in the adrenal glomerulosa, resulting in increased secretion of the steroid hormone aldosterone. Aldosterone binds to mineralocorticoid receptors in principal cells, leading to increased activity of the Source: The Inherited Basis of Blood Pressure Variation and Hypertension, The Online Metabolic and Molecular Bases of Inherited Disease epithelial sodium channel. Diseases caused by mutations in genes of these pathways are indicated. Citation: Valle D, Beaudet AL, Vogelstein B, Kinzler KW, Antonarakis SE, Ballabio A, Gibson K, Mitchell G. The Online Metabolic and Molecular Bases of Inherited Disease; 2014 Available at: http://mhmedical.com/ Accessed: August 09, 2017 Copyright © 2017 McGraw-Hill Education. All rights reserved
