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The presently accepted regulators of the homeostatic excretion of potassium are the plasma concentrations of aldosterone and potassium. Evidence for a role of aldosterone is reviewed, and it is pointed out that aldosterone is kaliuretic at supraphysiologic levels but has little kaliuretic activity within its normal secretory range. Elevation of plasma potassium above its normal range enhances the kaliuretic action of aldosterone. Elevation of plasma potassium above, but not within, its normal range is strongly kaliuretic. In sheep the kaliuresis induced by intake of a potassium rich meal cannot be explained by changes in aldosterone or plasma potassium. A kaliuretic reflex arising from receptors in the gut, portal vein or liver has been proposed the explain the meal-induced kaliuresis. This putative reflex involves the central nervous system and efferent kaliuretic factors other than aldosterone and plasma potassium. Evidence for the involvement of the central nervous system and undetermined kaliuretic regulatory factors can be found in studies of the physiologic circadian rhythm of renal potassium excretion. This rhythmic excretion does not appear to depend on changes in either aldosterone or plasma potassium.

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In unanesthetized adult sheep, following intake of a daily meal, there was a peak in K excretion. The maximum and minimum rates of K excretion following meals were directly related to meal K content. On days without meals, no peak in K excretion occurred. Changes in K excretion on fed and fast days occurred without changes in the low levels of plasma aldosterone and were poorly correlated with urine or blood pH, urine flow rate, Na excretion, or the filtered load of K, but they correlated well with fractional K excretion. Plasma K did not change on fast days. Plasma K increased on some, but not all, fed days. Increases in plasma K that occurred on fed days were insufficient to account for the concurrent kaliuresis. Infusion of aldosterone or isotonic NaCl failed to alter K excretion in fed or fasted sheep. Infusion of isotonic NaCl + aldosterone hypertonic Na2SO4 + aldosterone increased K excretion in fasted but not fed sheep. Infusion of K in the rumen of fed and fasted sheep elevated rumen K concentration and led to increases in K excretion that could not be explained by increases in plasma K. The mechanisms responsible for the homeostatic changes in K excretion on fed and fast days were not ascertained but may importantly depend on sensors of enteric K content.

To determine the quantitative relation of K excretion (UKV) to plasma K concentration (PK), three fasted, conscious, mature ewes were infused intravenously with 50 mmol KCl over 15, 30, and 60 min. Control experiments were without infusion. During KCl infusion PK was increased to 7.26 +/- 0.40 (15 min), 6.68 +/- 0.48 (30 min), and 5.59 +/- 0.3 meq/liter (60 min). During all three infusions the increase in UKV relative to the increase in PK was similar. The mean delta UKV/delta PK ratio was 160 +/- 30 (SD) mueq/min per meq/liter (range 102-203). On termination of each infusion PK decreased to control values, but UKV either remained elevated (60-min infusion) or first decreased and then increased (15- and 30-min infusions). The second, delayed kaliuresis began 30-45 min after initiation of KCl infusion and accelerated a return to the level of K balance of the control experiments. A plot of UKV against the corresponding period PK showed that, at a common value of PK, UKV was higher following KCl infusion when PK was dropping than during KCl infusion when PK was rising. The mechanisms responsible for this hysteresis phenomenon are not identified.

It has been known for decades that urinary potassium excretion varies with a circadian pattern. In this review, we consider the historical evidence for this phenomenon and present an overview of recent developments in the field. Extensive evidence from the latter part of the last century clearly demonstrates that circadian potassium excretion does not depend on endogenous aldosterone. Of note is the recent discovery that the expression of several renal potassium transporters varies with a circadian pattern that appears to be consistent with substantial clinical data regarding daily fluctuations in urinary potassium levels. We propose the circadian clock mechanism as a key regulator of renal potassium transporters, and consequently renal potassium excretion. Further investigation into the mechanism of regulation of renal potassium transport by the circadian clock is warranted in order to increase our understanding of the clinical relevance of circadian rhythms to potassium homeostasis.

Ingestion of potassium salts typically induces both a kaliuresis and an increase in the systemic plasma potassium concentration. In this study normal healthy adults undergoing water diuresis ingested potassium citrate or sodium citrate (0.5 mmol/kg body weight) or continued without ion ingestion (a time control group). Urine was collected over 20-min intervals and venous blood sampled at midinterval. Intake of potassium citrate led to a significant increase in potassium excretion that began during the first postingestion collection and peaked 60-80 min after intake with a maximal increase in potassium excretion above baseline of 1.60 μmol/min·kg^-1 The kaliuresis occurred without changes in plasma potassium concentration, excretion of creatinine or calcium, or urine hypo-osmolality and was associated with a briefer, smaller, and less regular increase in sodium excretion and a pronounced but irregular increase in chloride excretion. Plasma aldosterone was insignificantly elevated above baseline, and the initial increase did not occur until 40-60 min after potassium intake. Intake of sodium citrate did not produce a kaliuresis. The cause of the kaliuresis does not appear to be an increased systemic plasma potassium concentration, an increased plasma level of aldosterone, intake of citrate, or an elevated excretion of sodium. The mechanism inducing the kaliuresis following oral potassium intake in the absence of changes in systemic plasma potassium may involve a reflex initiated at potassium sensors in gut, portal vein, or liver.