Abstract
1 The overflow of endogenous noradrenaline from the rat mesenteric arterial vasculature was determined along with the perfusin pressure response to periarterial nerve stimulation (PNS) (4-12 Hz). 2 The PNS-induced pressor responses were blocked by prazosin at 3 .times. 10-8 M but not only by prazosin at 10-6 M or the combination of prazosin at 3 .times. 10-8 M and yohimbine (10-7 M). 3 The PNS-induced overflow of endogenous noradrenaline was significantly augmented by prazosin at 10-6 M or the combination of prazosin at 3 .times. 10-8 M and yohimbine (10-7 M) but not by prazosin at 3 .times. 10-8 M alone. 4 The PNS-induced pressor response and endogenous noradrenaline overflow, in the absence of prazosin, were not significantly influenced by .alpha., .beta.-methylene-adenosine triphosphate (.alpha., .beta.-methylene ATP) (3 .times. 10-6 M). The pressor responses to PNS which remained after prazosin at 10-6 M were abolished by pretreatment with .alpha., .beta.-methylene ATP and therefore attributable to coreleased ATP. 5. The pressor responses to exogenous noradrenaline were abolished by prazosin at both 3 .times. 10-8 M and 10-6 M. 6. These results suggest no functionally significant amount of ATP was coreleased with noradrenaline by PNS in the presence of prazosin at low concentrations which blocked only postjunctional .alpha.1-adrenoreceptors. 7 Thus, these results indicate that the effects of prazosin at high concentrations, such as 10-6 M, on sympathetic neurotransmission should not be ignored when considering the mechanisms of vasoconstrictor responses to PNS following high concentrations of prazosin.

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