PATTERN OF RENAL VASOCONSTRICTION AND TRANSMITTER RELEASE DURING SYMPATHETIC STIMULATION IN PRESENCE OF ANGIOTENSIN AND COCAINE

¹ Department of Pharmacology, University of Minnesota, Minneapolis, Minnesota

A preparation was devised in which the sympathetic vasoconstrictor response in the dog kidney perfused in vivo at constant blood flow could be elicited and measured, and the accompanying release of transmitter into the venous effluent could be quantitated. An i.a. infusion of angiotensin II amide resulted in potentiation of the response to sympathetic stimulation at a low frequency (2 cps) and an increased release of catecholamine elicited during stimulation at a higher frequency (5 cps). The vasoconstrictor response to sympathetic stimulation was increased to a much greater degree than the vasoconstrictor response to i.a. administered norepinephnine (1 µg). Cocaine, when infused i.a., potentiated the responses to both sympathetic stimulation and norepinephrine, the latter to a somewhat greater degree. Release of catecholamine during stimulation at the higher frequency also was increased after cocaine. The difference in the relative degree of potentiation of the response to endogenously released vs. exogenously administered catecholamine, and the characteristics of the potentiated response at the lower frequency after angiotensin, suggest that this potentiation is accounted for by a mechanism different from blockade of reuptake of the transmitter.

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