Saito M, Kato T, Kondo A, Miyake K
Department of Urology, Nagoya University School of Medicine.
Hinyokika Kiyo. 1992 May;38(5):525-30.
The response of the human detrusor muscle to angiotensins and the difference in contractility between neurogenic and control bladders were examined. Both angiotensin I and II induced potent contraction of the human detrusor muscle. In Ca-free Krebs' solution the contractile response to angiotensin II was abolished. However, verapamil and indomethacin suppressed it only slightly. Captopril blocked completely the response to angiotensin I, and saralasin inhibited completely the response to both angiotensin I and II. The contraction strength in response to both angiotensin I and II was significantly weaker in the neurogenic bladder than in the control. However, there was no difference in the value of ED50 between the two groups. These findings suggest that angiotensin I is converted to angiotensin II by angiotensin converting enzyme at the detrusor, and that angiotensin II subsequently contracts the detrusor muscle through angiotensin II receptors. The contractility of the neurogenic bladder in response to angiotensin was significantly lower compared to that of the control.
研究了人逼尿肌对血管紧张素的反应以及神经源性膀胱和对照膀胱之间收缩性的差异。血管紧张素I和II均能引起人逼尿肌的强烈收缩。在无钙的克雷布斯溶液中,对血管紧张素II的收缩反应消失。然而,维拉帕米和吲哚美辛仅轻微抑制该反应。卡托普利完全阻断了对血管紧张素I的反应,沙拉新完全抑制了对血管紧张素I和II的反应。神经源性膀胱对血管紧张素I和II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。这些发现表明,血管紧张素I在逼尿肌处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。与对照组相比,神经源性膀胱对血管紧张素的收缩性明显较低。