“…It has become clear that saralasin, particularly in sodium-replete conditions, may raise arterial pressure (Streeten et al, 1975;Case et al, 1976;Hollenberg, Williams, Burger, Ishikawa & Adams, 1976;McGregor & Dawes, 1976;Anderson, Streeten & Dalakos, 1977;Fagard et al, 1977a;Noth et al, 1977) and renal vascular resistance (Hollenberg et al, 1976), increase plasma aldosterone levels (Noth et al, 1977;Brown, Tucker, Tue, Wisgerhof & Salassa, 1978;Fagard, Lijnen, Amery & Reybrouck, 1978a;Williams, Hollenberg, Brown & Mershey, 1978;Agabiti-Rosei, Brown, Brown, Fraser, Trust, Lever, Morton & Robertson, 1979;Donker, Van Hoogdalem, Pratt & Leenen, 1979) and possibly suppress renin activity (Hollenberg et al, 1976;McGregor & Dawes, 1976;Noth et al, 1977;Williams et al, 1978). When plasma renin and angiotensin levels rise in response to sodium restriction blood pressure usually falls during saralasin (Brunner et aI., 1974;Streeten et al, 1975;Brown et al, 1976;Case et al, 1976;McGregor & Dawes, 1976;Fagard et al, 1977a;Noth et al, 1977;Posternak et al, 1977;Fagard et al, 1978c;Van Hoogdalem et al, 1978), plasma aldosterone decreases or remains unchanged (Brown et al, 1976;Noth et al, 1977;Brown et al, 1978;Fagard et al, 1978a;Williams et al, 1978;Agabiti-Rosei et al, 1979;Donker et aI., 1979;Williams, Hollenberg, Moore, Swartz & Dluhy, 1979) and ...…”