Nonadrenergic nature of prazosin-resistant, sympathetic contraction in the dog mesenteric artery.

Electrical transmural stimulation of the isolated dog mesenteric artery produced a contractile response which was abolished by guanethidine and 6-hydroxydopamine but not by prazosin. Approximately 60% of the response seen with a frequency of 3 Hz remained after the treatment with prazosin. The prazosin-resistant contraction induced by electrical transmural stimulation was potentiated by other alpha adrenoceptor antagonists (phentolamine, phenoxybenzamine, tolazoline and DG-5128). Alpha-2 adrenoceptor agonists (including norepinephrine) attenuated the prazosin-resistant contraction and this attenuation was antagonized by the alpha antagonists mentioned above. Cocaine slightly inhibited the prazosin-resistant contraction, whereas this drug markedly augmented the contractile response to electrical stimulation before treatment with prazosin. In reserpine-treated mesenteric arteries also, electrical transmural stimulation produced a contraction and this was neither suppressed nor potentiated by prazosin and other alpha antagonists but was attenuated by alpha-2 agonists. Guanethidine and 6-hydroxydopamine abolished the prazosin-resistant contraction in reserpine-treated arteries. Nicotine, but not tyramine, also produced such prazosin-resistant contraction in reserpine-treated and untreated arteries. Exogenous norepinephrine produced a concentration-dependent contraction in reserpine-treated and untreated arteries and the responses were competitively antagonized by prazosin. These results indicate that the prazosin-resistant contractions of the dog mesenteric artery induced by electrical transmural stimulation and nicotine are sympathetic in origin but not adrenergic in nature. Such prazosin- resistant contraction was observed in the dog mesenteric vein but not in carotid and femoral arteries, thereby suggesting that the nonadrenergic component may play an important role in the regulation of visceral blood flow.