Abstract
1. There is considerable evidence for the existence of an endogenous inhibitor of Na+/K(+)-ATPase. The exact physiological nature and role of this postulated agent remains unclear, although it would be predicted that one of its actions would be stimulation of renal sodium excretion. 2. The natriuretic effect of renal arterial infusion of ouabain is relatively slow in onset and is sustained. 3. The natriuresis is not modified by changes in sodium status, unlike the natriuretic effect of atrial natriuretic peptide. 4. The natriuretic action of ouabain is enhanced dramatically by acute volume expansion or chronic mineralocorticoid treatment, which both result in hypokalaemia, hypertension and hypervolaemia. 5. The natriuretic response to small increments in blood pressure is markedly enhanced by treatment with ouabain. 6. We hypothesize that the interaction between the inhibition of Na+/K(+)-ATPase and elevated blood pressure could result in the shedding of sodium in conditions where there are increased levels of circulating endogenous digitalis-like factors.
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