Prejunctional alpha adrenoceptor and angiotensin receptor function in isolated human, monkey and dog arteries.

Transmural electrical stimulation (2-20 Hz) produced a frequency-dependent contraction in dog mesenteric, monkey mesenteric and human gastroepiploic arterial strips, which was abolished by tetrodotoxin and suppressed by phentolamine. Treatment with yohimbine (10(-9) and 10(-8) M) potentiated the response to nerve stimulation dose-dependently in the dog arteries, but rather attenuated the response of the primate arteries. Yohimbine (10(-8) M) attenuated the contraction caused by exogenous norepinephrine in the dog and monkey arteries. Angiotensin (ANG) II (2 X 10(-10) M) and ANG I (10(-9) M) potentiated the response to transmural stimulation in the dog and monkey arteries, whereas the response to norepinephrine was unaffected. The ANG I-induced potentiation was suppressed by treatment with ANG converting enzyme inhibitors. 3H-Overflow evoked by transmural stimulation in tissues prelabeled with [3H] norepinephrine was increased by yohimbine in the superfused dog arteries but was not increased significantly in the monkey arteries. The overflow was increased significantly by ANG II in the dog and monkey arteries. It may be concluded that prejunctional alpha-2 adrenoceptors mediating the inhibition of transmitter release do not function significantly in human gastroepiploic and monkey mesenteric arteries, and postjunctional alpha-2 receptors are involved partly in contractions of the monkey arteries due to adrenergic nerve stimulation. ANG II appears to be synthesized from ANG I via ANG converting enzyme in the primate arteries; the octapeptide potentiates the contraction caused by adrenergic nerve stimulation, possibly due to prejunctional ANG receptor activation and increased norepinephrine release.