Department of Physiology, Semmelweis Medical University, H-1444 Budapest 8, Hungary
(Received 23 December 1975)
The role of the renin-angiotensin system (RAS) in the control of aldosterone secretion in the rat has been a subject for disagreement for more than a decade (cf. Müller, 1971). Recent investigations of the effect of synthetic angiotensin II on isolated glomerulosa cells (Haning, Tait & Tait, 1970; Brecher, Tabacchi, Pyun & Chobanian, 1973; Williams, McDonnell, Raux & Hollenberg, 1974; Mendelsohn, Mackie & Mee, 1975) failed again to give concordant results concerning even the efficiency of the octapeptide.
Information on the physiological function of the RAS may be obtained by experiments studying the response of aldosterone secretion rate to an evoked increase in endogenous renin activity. A situation where the RAS may be expected to play a mediator role in aldosterone regulation is the reduction of renal perfusion pressure. The effect of this manoeuvre on aldosterone
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