Abstract
The renal and cardiac adrenergic nerve patterns in rats infused with large and small amounts of angiotensin and in rats given NaCl plus DOCA [deoxycorticosterone acetate] NaCl alone and salt-free diets were examined by the histochemical fluorescence method. Infusion of small amounts of angiotensin led to a persistent blood pressure elevation, whereas infusion of large amounts of angiotensin transiently raised blood pressure, probably due to development of tachyphylaxis. Nerve patterns were normal in angiotensin-infused rats and in rats given NaCl. In rats given NaCl plus DOCA and in rats subjected to salt restriction, a partial or complete disappearance of the transmitter of the adrenergic nerve terminals were recorded. Angiotensin in itself is probably incapable of inducing visible alterations in the transmitter content of the terminals. The findings agree with the view that angiotensin potentiates a norepinephrine depletion of the terminals during sympathetic activity, since it can be assumed that increased plasma angiotensin levels and various degrees of increased sympathetic tonus were present in the rats subjected to salt restriction. The similar effect on the nerve terminals produced by the combined NaCl and DOCA administration is consistent with earlier reports of an increased turnover of norepinephrine in animals thus treated.