Ueda S, Yano S, Sakanashi M, Mutoh S, Ikegami K
Eur Urol. 1981;7(4):237-42. doi: 10.1159/000473227.
Actions of some autonomic drugs on upper, middle and lower portion of isolated dog ureters under quiescent state were investigated quantitatively. Noradrenaline and adrenaline at lower concentrations evoked contractions in each portion of the ureters and increased the concentration-dependent frequency and tension of these contractions, but attenuated them at higher concentrations. Phentolamine significantly depressed these contractions, while propranolol enhanced them. Phenylephrine increased the concentration-dependent frequency and tension of contractions, which were suppressed by phentolamine. Acetylcholine at higher concentrations produced contractions of the ureters, and phentolamine or hexamethonium suppressed them. The results indicate that ureteral contractions may be stimulated through an activation of alpha-adrenoceptors and be attenuated through an activation of beta-adrenoceptors, and that acetylcholine may release noradrenaline from sympathetic nerve endings through an activation of presynaptic nicotinic receptors, resulting in ureteral contractions.
定量研究了一些自主神经药物对处于静息状态的离体犬输尿管上、中、下部分的作用。低浓度的去甲肾上腺素和肾上腺素可引起输尿管各部分收缩，并增加这些收缩的浓度依赖性频率和张力，但在高浓度时则使其减弱。酚妥拉明显著抑制这些收缩，而普萘洛尔则增强它们。去氧肾上腺素增加收缩的浓度依赖性频率和张力，酚妥拉明可抑制这些作用。高浓度的乙酰胆碱可引起输尿管收缩，酚妥拉明或六甲铵可抑制它们。结果表明，输尿管收缩可能通过α-肾上腺素能受体的激活而被刺激，并通过β-肾上腺素能受体的激活而减弱，并且乙酰胆碱可能通过突触前烟碱受体的激活从交感神经末梢释放去甲肾上腺素，从而导致输尿管收缩。
