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OBJECTIVE Muscarinic (mAChRs) and nicotinic (nAChRs) acetylcholine receptors are both expressed in endothelial cells.It is generally accepted that mAChRs are responsible for both endothelium-dependent relaxations and contractions evoked by acetylcholine.The present study was designed to study whether or not nAChRs are also involved in endothelium-dependent relaxations.METHODS Rat aortic rings with or without endothelium were suspended in organ chambers for isometric tension recording.Quiescent rings were incubated with vehicle, mecamylamine (nAChRs inhibitor) , atropine (mAChRs inhibitor,) , mecamylamine plus atropine, L-NAME (NO synthase inhibitor) or TRAM-34 plus UCL-1684 (inhibitors of EDHF-mediated responses).All rings were incubated with indomethacin (non-selective cyclooxygenase inhibitor) to prevent endothelium-dependent contractions.After 40 minutes of incubation, they were contracted with phenylephrine and then relaxed with cumulatively increasing concentrations of acetylcholine or nicotine.RESULTS (1) In both SHR and WKY aortae, acetylcholine-induced relaxations were similar in control and mecamylamine-treated tings, while the relaxations were significantly reduced in atropine-treated preparations.In rings of 36 weeks old SHRs, the remaining response in the presence of atropine approximated 50% of those observed in untreated control preparations, and was prevented by mecamylamine.In both 36 weeks and 64 weeks old WKY aortae the remaining response in atropine-treated preparations was minimal.(2) In both SHR and WKY aortae, nicotine induced up to 60% endothelium-dependent relaxation and the relaxations were abolished by L-NAME.TRAM-34 plus UCL-1684 partially inhibited the nicotine-induced relaxations in WKY but not in SHR aorta.CONCLUSION In the SHR and WKY aorta, mAChRs are mainly responsible for endothelium-dependent relaxations under control conditions.However, when mAChRs are inhibited by atropine, nAChRs mediate relaxations to the cholinerglc transmitter in the SHR but not the WKY aorta.