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Research Article Free access | 10.1172/JCI106430

The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects

Hans R. Brunner, Leslie Baer, Jean E. Sealey, John G. G. Ledingham, and John H. Laragh

1Department of Medicine, Columbia University, College of Physicians and Surgeons and the Presbyterian Hospital in the City of New York, New York 10032

Find articles by Brunner, H. in: PubMed | Google Scholar

1Department of Medicine, Columbia University, College of Physicians and Surgeons and the Presbyterian Hospital in the City of New York, New York 10032

Find articles by Baer, L. in: PubMed | Google Scholar

1Department of Medicine, Columbia University, College of Physicians and Surgeons and the Presbyterian Hospital in the City of New York, New York 10032

Find articles by Sealey, J. in: PubMed | Google Scholar

1Department of Medicine, Columbia University, College of Physicians and Surgeons and the Presbyterian Hospital in the City of New York, New York 10032

Find articles by Ledingham, J. in: PubMed | Google Scholar

1Department of Medicine, Columbia University, College of Physicians and Surgeons and the Presbyterian Hospital in the City of New York, New York 10032

Find articles by Laragh, J. in: PubMed | Google Scholar

Published November 1, 1970 - More info

Published in Volume 49, Issue 11 on November 1, 1970
J Clin Invest. 1970;49(11):2128–2138. https://doi.org/10.1172/JCI106430.
© 1970 The American Society for Clinical Investigation
Published November 1, 1970 - Version history
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Abstract

The effect of potassium administration and of dietary potassium deprivation on plasma renin activity and aldosterone excretion has been studied in 10 normal subjects and in 12 hypertensive patients maintained on a constant dietary regimen.

Potassium administration reduced plasma renin activity in 18 of 28 studies of both normal and hypertensive subjects. Suppression of renin often occurred despite sodium diuresis induced by potassium administration. The renin suppression was related to induced changes in plasma potassium concentration and urinary potassium excretion.

The failure of suppression of plasma renin in 10 studies could be accounted for by the smaller amounts of potassium administered to these subjects, together with a possibly overriding influence of an induced sodium diuresis.

In six studies potassium deprivation invariably increased plasma renin activity even though a tendency for sodium retention often accompanied this procedure.

The data indicate that both the suppression of plasma renin activity induced by potassium administration and the stimulation of renin activity which follows potassium depletion occur independently of associated changes in either aldosterone secretion or in sodium balance. However, the results do suggest that in various situations, the influence of potassium on plasma renin activity may be either amplified or preempted by changes in sodium balance.

These interactions between potassium and plasma renin could be mediated by an ill-defined extrarenal pathway. But the findings are more consistent with an intrarenal action of potassium ions to modify renin release. Potassium might modify renin secretion directly by acting on the juxtaglomerular cells or by a change in its tubular reabsorption or secretion. The effects of potassium ions on renin secretion might also be mediated indirectly via an induced change in tubular sodium transport.

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