Saito M, Kondo A, Kato T, Miyake K
Department of Urology, Nagoya University School of Medicine, Japan.
J Urol. 1993 Feb;149(2):408-11. doi: 10.1016/s0022-5347(17)36105-0.
The response of the human detrusor muscle to angiotensins was investigated and compared between neurogenic and control bladders. Both angiotensin I and II induced potent contraction of the human detrusor muscle. Saralasin completely inhibited the response to both angiotensins, while verapamil and indomethacin barely suppressed the contractility provoked by angiotensin II. Captopril completely blocked the response to angiotensin I. The contractile response of angiotensin II was abolished in Ca(++)-free Krebs' solution. The contractile strength of the neurogenic bladders induced by both angiotensin I and II was significantly weaker than that of the controls. However, there was no difference in ED50 value between the 2 groups. These results support the hypothesis that angiotensin I is converted to angiotensin II by angiotensin converting enzyme in the detrusor, and that angiotensin II subsequently contracts the detrusor muscle through angiotensin II receptors. The bladder contractility induced by the angiotensins was significantly less potent in the neurogenic bladders than in the control.
研究了人类逼尿肌对血管紧张素的反应,并比较了神经源性膀胱和对照膀胱之间的差异。血管紧张素I和II均能引起人类逼尿肌强烈收缩。沙拉新完全抑制了对两种血管紧张素的反应,而维拉帕米和吲哚美辛几乎不能抑制血管紧张素II引起的收缩性。卡托普利完全阻断了对血管紧张素I的反应。在无钙的克雷布斯溶液中,血管紧张素II的收缩反应消失。血管紧张素I和II诱导的神经源性膀胱的收缩强度明显弱于对照组。然而,两组之间的半数有效量(ED50)值没有差异。这些结果支持以下假设:血管紧张素I在逼尿肌中被血管紧张素转换酶转化为血管紧张素II,随后血管紧张素II通过血管紧张素II受体使逼尿肌收缩。在神经源性膀胱中,血管紧张素引起的膀胱收缩性明显低于对照组。