The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects.
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.
D000328:Adult; D000450:Aldosterone / Q000378:metabolism*; D000804:Angiotensin II / Q000378:metabolism; D001693:Biological Transport, Active; D001794:Blood Pressure; D004035:Diet Therapy; D005260:Female; D006801:Humans; D006973:Hypertension / Q000378:metabolism* / Q000628:therapy; D007606:Juxtaglomerular Apparatus / Q000378:metabolism; D007668:Kidney / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D009318:Natriuresis; D011188:Potassium / Q000008:administration & dosage / Q000378:metabolism*; D011191:Potassium Deficiency / Q000378:metabolism*; D012083:Renin / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism
D000804:Angiotensin II; D000450:Aldosterone; D012964:Sodium; D012083:Renin; D011188:Potassium