Epinephrine facilitates neurogenic responses in isolated segments of dog mesenteric arteries.

Epinephrine (EPI) bitartrate (10(-9)-10(-8) M) significantly enhanced tension development in response to electrical field stimulation in isolated segments of dog mesenteric arteries. Responses to exogenous norepinephrine (NE) were generally unaffected, indicating that the EPI-induced increases in response to field stimulation are not explicable in terms of changes in postjunctional sensitivity. The facilitatory effects of EPI (5 X 10(-9) M) were unaffected by atenolol (10(-6) M) but were completely abolished by timolol (2 X 10(-7) M), suggesting an involvement of beta 2-adrenoreceptors in mediating the EPI-induced facilitation of neurogenic responses. Responses to exogenous NE were usually unaffected by either beta-adrenoreceptor antagonist. The results suggest that release of endogenous sympathetic neurotransmitter, measured in terms of postjunctional effects on vascular smooth muscle tone, appears to be modulated by prejunctional facilitatory beta 2-adrenoreceptors and that these receptors may be a physiologic site of action of EPI.