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Allen Sugarman, MD; Thomas Kahn, MD
Veterans Administration Medical Center Bronx, NY Mount Sinai School of Medicine New York

JAMA. 1988;259(4):519-520.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—Recent letters to JAMA have discussed the issue of hyperkalemia in association with the use of calcium channel antagonists.^1,2 The link between calcium and potassium transport at the cellular level has been well recognized. Membrane permeability to potassium in many cell types has been shown to be related to the concentration of intracellular calcium.³ Studies have revealed that maneuvers designed to increase effective intracellular calcium concentration enhance net potassium efflux from cells,⁴ whereas those directed at reducing effective intracellular calcium concentration impair net potassium efflux from cells.⁵

Our studies have shown that verapamil and nifedipine enhance the extrarenal disposal of an acute intravenous potassium load administered to acutely nephrectomized rats.⁶ This enhanced extrarenal potassium tolerance could not be accounted for by the intervention of insulin, aldosterone, or β₂-catecholamines. We postulated that the impaired calcium entry into cells mediated by the . . . [Full Text PDF of this Article]

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