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

机译:正常和高血压受试者施钾和缺钾对血浆肾素的影响

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摘要

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.
机译:已在10名正常受试者和12名采用固定饮食方案的高血压患者中研究了施用钾和饮食中钾缺乏对血浆肾素活性和醛固酮排泄的影响;在两项均正常的28项研究中,施用钾可降低血浆肾素活性和高血压的对象。尽管通过钾施用引起钠利尿,但经常发生肾素抑制。肾素的抑制与血浆钾浓度的变化和尿中钾的排泄有关。在10项研究中,血浆肾素的抑制失败可能是由于给予这些受试者的钾量较少,以及在六项研究中,尽管钠保留的趋势经常伴随此过程,但钾缺乏总是不变地增加血浆肾素活性。数据表明,施用钾可抑制血浆肾素活性,而钾后刺激肾素活性贫血的发生与醛固酮分泌或钠平衡的相关变化无关。然而,结果确实表明,在各种情况下,钾对血浆肾素活性的影响可能会因钠平衡的变化而被放大或被抵消,而钾与血浆肾素之间的相互作用可能是由一个不清楚的肾外途径介导的。但是这些发现与钾离子改变肾素释放的肾脏内作用更为一致。钾可能通过作用于肾小球细胞或改变其肾小管的重吸收或分泌而直接改变肾素的分泌。钾离子对肾素分泌的影响也可能通过肾小管钠转运的诱导变化间接介导。

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