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Molecular Mechanisms Linking Salt to Hypertension
1Department of Physiology and Biomedical Engineering, Mayo Clinic, College of Medicine, Rochester, Minnesota; 2Department of Pharmacology, University of Hong Kong, Hong Kong, China; and 3Departement Angiologie, Institut de Recherches Servier, Suresnes, France
Submitted 7 July 2005 ; accepted in final form 16 September 2005
Unlike sodium, potassium is vasoactive; for example, when infused into the arterial supply of a vascular bed, blood flow increases. The vasodilation results from hyperpolarization of the vascular smooth muscle cell subsequent to potassium stimulation by the ion of the electrogenic Na+-K+ pump and/or activating the inwardly rectifying Kir channels. In the case of skeletal muscle and brain, the increased flow sustains the augmented metabolic needs of the tissues. Potassium ions are also released by the endothelial cells in response to neurohumoral mediators and physical forces (such as shear stress) and contribute to the endothelium-dependent relaxations, being a component of endothelium-derived hyperpolarization factor-mediated responses. Dietary supplementation of potassium can lower blood pressure in normal and some hypertensive patients. Again, in contrast to NaCl restriction, the response to potassium supplementation is slow to appear, taking 
4 wk. Such supplementation reduces the need for antihypertensive medication. "Salt-sensitive" hypertension responds particularly well, perhaps, in part, because supplementation with potassium increases the urinary excretion of sodium chloride. Potassium supplementation may even reduce organ system complications (e.g., stroke).
endothelium-derived hyperpolarization factor; Na+-K+-ATPase; potassium channels
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