Postsynaptic alpha adrenergic mechanisms were compared in cerebral and mesenteric arteries isolated from the baboon. The contractile response to norepinephrine (NE) of the cerebral artery was potent and similar to that of the mesenteric artery. The EC50 was 3.1 (2.0-5.0) X 10(-7) M for the cerebral artery and 2.6 (1.5-4.8) X 10(-7) M for the mesenteric artery. The maximum contraction expressed as a force developed/cross-sectional area did not differ between the two arteries, whereas that expressed as percentage of 30 mM KCl-induced contraction in the cerebral artery (118 +/- 9%) was less than in the mesenteric artery (145 +/- 6%). Phenylephrine produced a contraction in a manner similar to NE, although the EC50 values in both arteries were 2 to 3 times as large as those for NE. Clonidine produced a moderate contraction in the mesenteric artery (35 +/- 8% of the KCl-induced contraction) but no contraction in the cerebral artery. NE-induced contraction in the cerebral artery was inhibited more prominently by prazosin, a selective alpha-1 adrenoceptor antagonist, than that in the mesenteric artery; the pA2 value for prazosin in the cerebral artery was higher (9.70) than that in the mesenteric artery (8.95). In contrast, there was no difference in pA2 values for either phentolamine or yohimbine between the two arteries. Clonidine-induced contraction in the mesenteric artery was attenuated by prazosin rather than yohimbine at the same concentration used. Thus, it may be concluded that contractile processes related to postsynaptic alpha-1 adrenoceptor stimulation are predominantly operative in baboon cerebral and mesenteric arteries, the cerebral artery being more susceptible to the inhibitory effect of prazosin.