Abstract

We have used the blood-bathed organ technique (Vane 1964) to study the liberation of renin into the bloodstream and the subsequent formation of angiotensin I and angiotensin II. The rat isolated colon was superfused (Gaddum 1953) continuously with heparinized blood from dogs, to detect changes in angiotensin II concentration in the blood (Regoli & Vane 1964, 1966). The release of renin from the kidney can be induced either by a large fall in perfusion pressure (Skinner, McCubbin & Page 1963; Regoli & Vane 1966) or by haemorrhage (Scornik & Paladini 1964) The fact that a slow haemorrhage can induce secretion of renin without a fall in arterial blood pressure (Hodge, Lowe & Vane 1966 a ) led to experiments which showed that secretion of renin is under reflex control; one afferent limb of the reflex probably originates in stretch receptors in the venous or low pressure side of the circulation and is mediated by afferent nerves in the vagus. The efferent pathway is the renal sympathetic supply (Hodge, Lowe & Vane 1966 a , b ).

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