Salt handling and hypertension
Kevin M. O’Shaughnessy, Fiona E. Karet
Kevin M. O’Shaughnessy, Fiona E. Karet
Published April 15, 2004
Citation Information: J Clin Invest. 2004;113(8):1075-1081. https://doi.org/10.1172/JCI21560.
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Science in Medicine

Salt handling and hypertension

Abstract

The kidney plays a central role in our ability to maintain appropriate sodium balance, which is critical to determination of blood pressure. In this review we outline current knowledge of renal salt handling at the molecular level, and, given that Westernized societies consume more salt than is required for normal physiology, we examine evidence that the lowering of salt intake can combat hypertension.

Authors

Kevin M. O’Shaughnessy, Fiona E. Karet

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Figure 1

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The renin-angiotensin-aldosterone axis and molecular pathways of sodium ...
The renin-angiotensin-aldosterone axis and molecular pathways of sodium reabsorption in the nephron. A cartoon of a nephron is shown, with sodium-reabsorbing cells of the thick ascending limb of the loop of Henle (TALLH), distal convoluted tubule (DCT), and collecting duct (CD). The latter is responsible for fine regulation via the aldosterone-activated mineralocorticoid receptor (MR). In all cells, sodium exits the basolateral compartment via the Na/K-ATPase (not shown). Aldosterone synthesis is controlled by angiotensin II. Numbers reflect cellular components affected in disorders of sodium homeostasis referred to in the text: 1, Liddle syndrome; 2a/b, recessive/dominant PHA1; 3a/b/c/d, types I/II/III/IV Bartter syndrome; 4, Gitelman syndrome; 5, Gordon syndrome. *Sites of action of antihypertensive drugs. ROMK2, renal outer medullary potassium channel.