Vasomotor effects of noradrenaline, 5-hydroxytryptamine, angiotensin II, bradykinin, histamine, and acetylcholine on the bat (Rhinolophus ferrumequinum) basilar artery.

The responsiveness of the basilar artery to intrinsic vasoactive substances is species-specific and can be a unique characteristic. We investigated the responsiveness of the bat (Rhinolophus ferrumequinum) basilar artery to noradrenaline (NA), 5-hydroxytryptamine (5-HT), angiotensin (Ang) II, bradykinin (BK), histamine (His), and acetylcholine (ACh). NA, 5-HT, Ang II, and BK induced contraction, whereas His and ACh induced relaxation, in a concentration-dependent manner. The NA cumulative concentration-response curve was shifted to the right in parallel with phentolamine (an α-antagonist). However, propranolol, a β-antagonist, had no significant effect. The 5-HT curve was shifted to the right in parallel by ketanserin (a 5-HT ₂ antagonist) and methiothepin (a 5-HT ₁ and 5-HT ₂ antagonist). Losartan (an AT ₁ antagonist) shifted the Ang II curve to the right, whereas PD123319 (an AT ₂ antagonist) had no significant effect. L-NA, indomethacin, and des-Arg ⁹ -[Leu ⁸ ]-BK (a B ₁ antagonist) did not significantly affect BK-induced contractions. HOE140 (a B ₂ antagonist) shifted the BK concentration-response curve to the right. The His curve was shifted to the right weakly by diphenhydramine (an H ₁ antagonist) and strongly by cimetidine (a H ₂ antagonist). ACh-induced relaxation was significantly inhibited by L-NA, atropine, and pFHHSiD (a muscarinic M ₃ antagonist), whereas pirenzepine and methoctramine (muscarinic M ₁ and M ₂ antagonists, respectively) showed no significant effects. At a resting vascular tone, L-NA-induced contraction and indomethacin induced relaxation. These results suggest that α-adrenergic, 5-HT ₁ , 5-HT ₂ , AT ₁ , and B ₂ receptors might be important in arterial contraction, whereas M ₃ and H ₂ (>H ₁ ) receptors might modify these contractions, inducing relaxation.
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