Abstract
Preston et al. report urinary potassium excretion in healthy subjects in response to an acute potassium load with or without a meal. The investigators show a rapid kaliuretic response that occurs independently of the serum potassium and plasma aldosterone concentration, and that persists in the presence of a mineralocorticoid receptor blocker. This Commentary puts these data in perspective by reviewing the current understanding of the feedback and feedforward systems that regulate renal potassium excretion.
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