
Regulation of the Cl−/HCO−3HCO3− exchanger pendrin has been suggested to explain the aldosterone paradox. Therefore, a high-K+ diet has been proposed to downregulate a pendrin-mediated K+-sparing NaCl reabsorption pathway to maximize urinary K+ excretion. This study outlined that different dietary potassium salts differentially regulate pendrin and that its regulation is prioritized by the dietary anion, providing a mechanism to prevent metabolic alkalosis with high-K+ based diets and safeguard against hyperchloremic acidosis with consumption of high-KCl diets.
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