Potassium deficiency has long attracted the attention of both clinicians and physiologists because of its numerous effects on renal function. Since potassium is the most prevalent intracellular cation, it is not surprising that its deficiency results in marked alterations in cell structure and function. The most common abnormality of renal function is a concentrating defect, due to decreased solute concentration in the medulla and the unresponsiveness of the collecting tubule to vasopressin. This resistance to vasopressin is caused by increased prostaglandin production and the consequent prostaglandin-mediated inhibition of adenylate cyclase activation by vasopressin.1 Potassium deficiency is also associated with increased.
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