Activation of nicotinic receptors contributes to acetylcholine induced endothelium‐denpendent relaxations in rat aorta

The present study was designed to investigate whether or not nicotinic receptors (nAChRs) are involved in endothelium‐dependent relaxations evoked by acetylcholine. Male spontaneous hypertensive rats (SHR, 36 weeks) and Wistar Kyoto rats (WKY, 36 weeks & 64 weeks), and both female and male Sprague‐Dawley rats (SD, 30 weeks) were used. The aortic rings were incubated with vehicle, mecamylamine (nAChRs inhibitor), atropine [muscarinic receptor (mAChRs) inhibitor], or the combination of the two inhibitors, and then exposed to cumulatively increasing concentrations of acetylcholine to trigger relaxations. The results demonstrated that in SHR, WKY and SD aortae, acetylcholine‐induced relaxations were similar in control and mecamylamine‐treated rings, while the relaxations were significantly reduced in atropine‐treated preparations. In rings of 36 weeks old male SHRs, the remaining acetylcholine‐induced relaxations in the presence of atropine approximated 50% of control preparations, while the remaining response in atropine‐treated preparations was minimal in 36 weeks and 64 weeks old WKY and in 30 weeks male SD, and averaged 40% of control preparations in 30 weeks old female SD. The remaining response was nearly abolished by the combination of atropine plus mecamylamine In conclusion, mAChRs are mainly responsible for endothelium‐dependent relaxations to acetylcholine under control conditions in the rat aorta. However, when mAChRs are inhibited by atropine, nAChRs mediate relaxation to the cholinergic transmitter in male SHR and female SD but not in male WKY and SD. Thus activation of nAChRs contributes to acetylcholine induced endothelium‐dependent relaxations in aorta of hypertensive and female rats but not male healthy rats. Supported by research grand of the university of Hong Kong