Vasomotor Effects of Acetylcholine, Bradykinin, Noradrenaline, 5-Hydroxytryptamine, Histamine and Angiotensin II on the Mouse Basilar Artery

We investigated the responsiveness of the mouse basilar artery to acetylcholine (ACh), bradykinin (BK), noradrenaline (NA), 5-hydroxytryptamine (5-HT), histamine (His) and angiotensin (Ang) II in order to characterize the related receptor subtypes in vitro. ACh and BK induced endothelium-dependent relaxation of precontracted arteries with U-46619 (a thromboxane A(2) analogue). Atropine (a nonselective muscarinic receptor antagonist) and N omega-nitro-L-arginine (a NO synthase inhibitor, L-NNA) shifted the concentration-response curve for ACh to the right, whereas pirenzepine, methoctramine and pFHHSiD (muscarinic M-1, M-2 and M-3 antagonists, respectively) had no significant effect. L-NNA and HOE140 (a B-2 antagonist) shifted the concentration-response curve for BK to the right, whereas des-Arg(9)-[Leu(8)]-BK (a B-1 antagonist) and indomethacin (a cyclooxygenase inhibitor) had no significant effect. NA failed to produce any vasomotor action. His and Ang II induced concentration-dependent contraction. Diphenhydramine (a H-1 antagonist) shifted the concentration-response curve for His to the right, whereas cimetidine (a H-2 antagonist) had no significant effect. Losartan (an AT(1) antagonist) shifted the concentration-response curve for Ang II to the right, whereas PD 123319 (an AT(2) antagonist) had no significant effect. These results suggest that the H-1 and AT(1) receptor subtypes might play an important role in arterial contraction, whereas muscarinic receptor subtypes apart from M-1, M-2 and M-3, and B-2 receptors on the endothelium, might modify these contractions to relaxations.