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Myocardial function and subcellular calcium metabolism in chronic potassium deficiency.

Myocardial contractility was examined in whole, perfused hearts and in right ventricle papillary muscles of chronic K-depleted cats. Mitochondrial and sarcoplasmic reticulum (SR) calcium binding and concentration were estimated in the perfused hearts after exposure to 45Ca. In vitro SR Ca uptake was measured by the Millipore technique. Myocardial contractility was depressed in chronic potassium depletion and the degree of depression was related to the reduced SR Ca binding. These experiments suggest altered subcellular Ca metabolism as being a mechanism of depressed myocardial contractility in chronic K depletion.

Animals↗

Effect of potassium deficiency and gossypol on urinary N-acetyl-beta-glucosaminidase excretion in the rat.

Some men receiving gossypol in China developed elevated urinary N-acetyl-beta-glucosaminidase (NAG) levels and hypokalemia. Since idiopathic hypokalemia occurs in China, hypokalemic nephropathy may have caused the elevated NAG levels. To learn if gossypol is directly nephrotoxic, we treated rats with a normal or low potassium diet with or without gossypol. The low potassium diet produced high NAG levels rather than the gossypol. This indicates the importance of differentiating hypokalemic nephropathy from drug nephrotoxicity in regions where idiopathic hypokalemia occurs.

Acetylglucosaminidase↗