Thirty-nine decerebrate rabbits, curarized and maintained by artificial ventilation, were used in the experiments. In a control group which received only saline intravenous infusions, arterial pressure remained virtually unchanged for 6 h after decerebration. Three other groups were used, all of which received intravenous infusions of aldosterone starting 1 h after decerebration and continuing for 5 h: in these groups the pressure 1 h after decerebration was taken as 100%. In a group of animals which received a normal diet before the acute experiment, the mean percentage pressure rise at the end of 5 h of aldosterone infusion was 20·0 ± 2·3 (s.e.m.)%. In a group whose drinking water had been replaced with 1% NaCl solution, the mean percentage pressure rise after 5 h was 29·6 ± 3·2. In a group pretreated with a low salt intake, the mean percentage pressure rise after 5 h was 10·3 ± 2·8%. These results show that intravenous infusions of aldosterone at the rate of 6 μg/kg/h can raise arterial pressure in acute experiments, and that varying the sodium intake can alter the responsiveness of the cardiovascular system to the hypertensive action of aldosterone.
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