Renal Adaptation to a High Potassium Intake

Abstract

A B S T R A C T The influence on urinary acidification of prolonged ingestion of a high potassium diet was explored in normal men and dogs. In men, the response to acute ingestion of ammonium chloride was assessed in a paired fashion after 5 days of ingesting a formula diet of normal or high potassium content; whereas in animals chronically ingesting a small amount of hydrochloric acid, the response to an increase in daily potassiunm intake was assessed. Urine pH was lower in the potassium-loaded state with both these models, and the effect persisted in the dog studies as long as a high potassium intake was continued. The decrease in urine pH could not be accounted for by changes in plasma acid-base status, net acid excretion, rate of urine flow, urine ionic strength, or fixed buffer excretion, i.e., phosphate, creatinine, or organic acids. Studies of men with administration of exogenous aldosterone and studies of adrenalectomized dogs with constant, maintenance steroid replacement indicated that the decrease in urine pH does not result from altered aldosterone secretion.In the human studies the largest decreases in urine pH were associated with a concomitant diminution in both ammonium and net acid excretion, suggesting a primary decrease of ammonia diffusion into the urine. These events during potassium loading, which are the mirror image of changes during potassium depletion, suggest that the relation between potassium, urine acidification, and ammonia metabolism may play an important role. in the maintenance of hydrogen ion and possibly potassium homeostasis during alterations in potassium intake.Preliminary reports appeared in the Abstracts of the American Society of Nephrology, 1971. 5: 80. and CliGu. Res. 1972. 20: 612, 613. Dr. Tannen is an Established Investigator of The American Heart Association.Received for publication 13 June 1972 and in revised formt 12 February 1973. INTRODUCTIONThe acute administration of a potassium load results in an alkaline diuresis, presumably the result of an interaction between renal handling of potassium and hydrogen ion. It has been speculated that these ions are secreted in a competitive fashion (1) and that the mechanism involves a decrease in renal tubular cellhydrogen ion content (2, 3).On the other hand, urinary acidification after the chronic ingestion of a high potassium intake has received little attention. This seemed particularly cogent in light of recent studies of urinary acidification during potassium depletion that suggested an interaction between potassium regulation and renal ammonia production (4). The possibility that this mechanism might also play a role in the adaptive response to potassium loading was of interest, especially since the process leading to enhanced renal potassium excretion during chronic ingestion of a high potassium intake is currently undefined (3,(5)(6)(7). Therefore, urinary acidification was explored during chronic potassium loading in normal men and dogs. In contrast to acute administration, chronic potassium loading resulted ...

Control of Acid Excretion by the Kidney

“…Thus hyperkalemia may dimin ish ammonia production but not decrease net acid excretion, if the quantity of anion excreted without sodium is increased. However, in this case a greater fraction of cation excretion is accounted for by potassium than hydrogen ion, consistent with the hypothesis that inhibition of ammonia production by hyperkalemia can facilitate potassium excretion (58). Simi larly, potassium depletion can increase ammonia production but not in crease acid excretion if sodium-free anion excretion is decreased (64).…”

“…Potassium depletion, apparently even of minimal degree, stimu lates renal ammonia production (55-57); ingestion of a high potassium diet, or potassium retention induced in other fashions, appears to diminish renal ammonia production (57)(58)(59)(60)(61)(62). In addition, it appears that when ammonia production alters ammonium excretion it also modifi es potassium excretion.…”

Changes in Renal Haemodynamics and Electrolyte Excretion During Acute Hyperkalaemia in Conscious Adrenalectomized Sheep

“…The higher rates of hydrion excretion and the lower rates of bicarbonate excretion in the second and third experiments, relative to the first, would be consistent with this explanation. The urinary pH of acid-loaded men and dogs has been found to be depressed by high dietary potassium intake but no increase in aldosterone secretion appeared to be necessary for the effect [Tannen, Wedell and Moore, 1973]. Although 1-5 mg DOCA was the lowest level of mineralocorticoid which would reliably maintain the sheep for 24 hr it can be argued that since mineralocorticoid levels were in the range of sodium-depleted sheep (as indicated by the fall in the salivary sodium/potassium ratio) for part of any 24 hr this level of steroid supplementation was in reality a high level of maintenance.…”

Mechanisms in Hyperkalemic Renal Tubular Acidosis

“…This was interpreted as being due to decreased renal ammonia production. 20,21 In the presence of normal aldosterone production, however, a high intake of K ϩ does not commonly lead to metabolic acidosis per se in humans compared with rodents, in which dietary manipulation results in a much bigger K ϩ load. Reduction in ammonia production in humans is offset by an increase in distal sodium delivery and aldosterone upregulation, which promote K ϩ and H ϩ excretion as discussed already.…”