Hypertension is a global burden and a major contributor to cardiovascular disease and premature death. Public health guidelines for the management of high BP contain numerous dietary recommendations, of which one is a reduction in salt (NaCl) intake. In addition, the modern diet is also characterized by low potassium (K + ) content and recent guidelines propose increasing K + intake as an alternative or complementary measure to reducing salt intake for lowering of BP. Most beneficial effects of K + supplementation on BP involve a homeostatic response of the kidney to dietary-induced changes in extracellular K + concentrations, particularly decreased reabsorption of NaCl in the distal convoluted tubule. However, the effects of greater K + intake on BP are not linear, and the ideal K + supplementation or intake for management of BP remains unclear. This article covers the mechanisms in the kidney by which changes in K + translate to alterations in BP, the effects of altered K + intake in animal models and human populations, and the importance of concurrent salt intake and what constitutes K + supplementation.
Keywords: BP; aldosterone; cell and transport physiology; distal tubule; hypertension; ion transport; renal cell biology; renin-angiotensin system; tubular physiology.
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