Altiere R J, Kiritsy-Roy J A, Catravas J D
J Pharmacol Exp Ther. 1986 Feb;236(2):535-41.
Acetylcholine has been reported to produce vasodilation or vasoconstriction in the pulmonary circulation of different species. In rabbit lungs, acetylcholine is a potent vasoconstrictor. The present study was undertaken to examine the contractile effects of acetylcholine in arteries isolated from various regions of the rabbit pulmonary vascular bed and in thoracic aorta. Arteries isolated from within the lung were more responsive than extrapulmonary arteries (main pulmonary artery and aorta) to the contractile effects of acetylcholine. In vessels precontracted with norepinephrine, acetylcholine caused biphasic (relaxation-contraction) concentration-response curves. Atropine inhibited acetylcholine-induced contractions in all vessels, whereas pretreatment with cyclooxygenase or thromboxane synthetase inhibitors abolished contractile responses to acetylcholine only in intrapulmonary arteries. In accordance with these findings, acetylcholine caused a 3-fold increase in thromboxane A2 release from intrapulmonary arteries but not from extrapulmonary arteries. Inhibition of thromboxane synthetase abolished this effect of acetylcholine. Endothelium removal decreased contractile responses in intrapulmonary arteries but it did not decrease contractions in extrapulmonary arteries, suggesting that endothelium may contribute to acetylcholine-induced, thromboxane-mediated contractions in intrapulmonary arteries. Indomethacin did not inhibit contractile responses in endothelium-denuded main pulmonary artery or aorta but it abolished the weak contractile responses in intrapulmonary arteries without endothelium, indicating that arterial smooth muscle also was a source of contractile prostanoid biosynthesis enhanced by acetylcholine. These results demonstrate that acetylcholine contracts rabbit intrapulmonary arteries through generation of thromboxane A2 but that a different mechanism is responsible for mediating weaker acetylcholine-induced contractions in extrapulmonary artery and aorta.(ABSTRACT TRUNCATED AT 250 WORDS)
据报道，乙酰胆碱在不同物种的肺循环中可引起血管舒张或收缩。在兔肺中，乙酰胆碱是一种强效血管收缩剂。本研究旨在检测乙酰胆碱对从兔肺血管床不同区域分离的动脉以及胸主动脉的收缩作用。从肺内分离的动脉比肺外动脉（主肺动脉和主动脉）对乙酰胆碱的收缩作用更敏感。在用去甲肾上腺素预收缩的血管中，乙酰胆碱引起双相（舒张 - 收缩）浓度 - 反应曲线。阿托品抑制所有血管中乙酰胆碱诱导的收缩，而用环氧化酶或血栓素合成酶抑制剂预处理仅消除肺内动脉对乙酰胆碱的收缩反应。根据这些发现，乙酰胆碱使肺内动脉血栓素A2释放增加3倍，但肺外动脉未出现这种情况。抑制血栓素合成酶可消除乙酰胆碱的这种作用。去除内皮可降低肺内动脉的收缩反应，但不会降低肺外动脉的收缩反应，这表明内皮可能参与乙酰胆碱诱导的、血栓素介导的肺内动脉收缩。吲哚美辛不抑制去内皮主肺动脉或主动脉的收缩反应，但可消除无内皮肺内动脉的微弱收缩反应，表明动脉平滑肌也是乙酰胆碱增强的收缩性前列腺素生物合成的来源。这些结果表明，乙酰胆碱通过生成血栓素A2使兔肺内动脉收缩，但介导肺外动脉和主动脉中较弱的乙酰胆碱诱导收缩的机制不同。（摘要截短至250字）
