Why the study?
Does saralasin infusion affect plasma aldosterone concentration in hypertensive patients under varying sodium states?
Does saralasin infusion affect plasma aldosterone concentration in hypertensive patients under varying sodium states?
Saralasin acts as a competitive antagonist of the endogenous renin-angiotensin system on the adrenal cortex, demonstrating that sodium depletion's effect on aldosterone is largely mediated by the renin-angiotensin system.
Supports RAS mediation of aldosterone response to sodium depletion; hypothesis-generating for saralasin, needs randomized trials before any clinical consideration.
The effect of a 4-hour infusion of the angiotensin II analogue sar1 ala8 angiotensin II (saralasin) on plasma aldosterone concentration (PAC) was assessed in relation to plasma renin activity (PRA) in 12 patients, both on normal sodium intake and after marked sodium depletion. On normal sodium intake the response of PAC to saralasin was variable; following sodium depletion saralasin induced a marked decrease in PAC in 11 of 12 patients. The extent of the change in PAC induced by saralasin correlated closely with log PRA. The data indicate that saralasin is also a competitive antagonist of the effect of the endogenous renin-angiotensin system (RAS) on the adrenal cortex, with agonistic activity appearing at low levels of PRA. The effect of sodium depletion on AC appears to be mediated to a major degree by the RAS.
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Donker et al. (1979) studied this question.
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