1. Angiotensin II blockade before and after marked sodium depletion in patients with hyperten sion [unilateral renovascular (eight), bilateral renovascular (four) and essential (four)] was performed by intravenous administration of the angiotensin II antagonist Sar'-Ala 8 -angiotensin II (saralasin).2. On normal sodium intake, saralasin decreased mean blood pressure by 8 mmHg in the unilateral renovascular group, by 6 mmHg in the bilateral renovascular group and increased it by 3 mmHg in the essential hypertensive group. After sodium depletion saralasin decreased mean blood pressure by 33 mmHg, 35 mmHg and 18 mmHg respec tively. The saralasin-induced decrease in blood pressure significantly correlated with the log of the initial plasma renin activity.3. Saralasin infusion decreased effective renal plasma flow (ERPF) in all three hypertension sub groups, both on normal sodium intake and after sodium depletion. Glomerular filtration rate de creased in direct relation to the hypotensive effect of saralasin but ERPF showed this relationship only after sodium depletion. On normal sodium intake saralasin increased filtration fraction by 17%, but decreased it by 7% after sodium depletion.4. It is concluded that the hypotensive action of saralasin closely correlates with the value of circulating plasma renin activity, apparently in dependent of the aetiology of the hypertension. The Correspondence: Dr A. J. M. Donker, decrease in ERPF during saralasin infusion in the patients on normal sodium intake seems mainly related to the agonistic activity of saralasin, but that after sodium depletion to the hypotensive effect of saralasin.
This case report describes a patient with malignant hypertension and phaeochromocytoma in whom blockade of angiotensin II receptors by the competitive antagonist 1‐sar‐8‐ala‐angio‐tensin II (Saralasin®) resulted in a partial correction of the elevated BP. Plasma renin activity was high and rose further during the blockade. Competitive inhibition of angiotensin II by Saralasin does not abolish the pressor effect of catecholamines. It was therefore interesting to observe that in this patient with phaeochromocytoma, independently, both α‐adrenergic receptor blockade and angiotensin II receptor blockade were effective in lowering BP.
ABSTRACT. 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 PAC appears to be mediated to a major degree by the RAS.
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