De Jonge A, Wilffert B, Thoolen M J, Timmermans P B, van Zwieten P A
Life Sci. 1984 Apr 9;34(15):1433-9. doi: 10.1016/0024-3205(84)90057-2.
The present study describes a differential inhibitory effect of captopril and [Sar1 Ala8]angiotensin II (saralasin) on the neurogenic vasoconstriction in pithed normotensive rats. In pithed normotensive rats with intact kidneys captopril more profoundly inhibited the vasopressor response to spinal stimulation than observed for saralasin. Bilateral nephrectomy also diminished the hypertensive response to spinal stimulation. After bilateral nephrectomy, 1 h previously, captopril but not saralasin diminished the hypertensive response to spinal stimulation. After bilateral nephrectomy, 18-24 h previously, captopril did not produce an additional reduction of the vasopressor response to spinal stimulation. In contrast, saralasin significantly potentiated the neurogenic vasoconstriction. The results suggest that both captopril and saralasin diminish the hypertensive response to spinal stimulation by producing dilatation of vascular smooth muscle in pithed normotensive rats. Apart from this common mechanism, a differential effect of captopril and saralasin on the neurogenic vasoconstriction can be observed. In contrast to saralasin, captopril may depress the neurogenic vasoconstriction in pithed normotensive rats by blocking the sympathofacilitatory action induced by subpressor levels of angiotensin II (AII). In pithed normotensive rats, saralasin may mimic the sympathofacilitatory action of subpressor AII.
本研究描述了卡托普利和[Sar1 Ala8]血管紧张素II（沙拉新）对脊髓麻醉的正常血压大鼠神经源性血管收缩的不同抑制作用。在肾脏完整的脊髓麻醉正常血压大鼠中，卡托普利比沙拉新更能显著抑制对脊髓刺激的升压反应。双侧肾切除也减弱了对脊髓刺激的高血压反应。在双侧肾切除1小时前，卡托普利可减弱对脊髓刺激的高血压反应，而沙拉新则无此作用。在双侧肾切除18 - 24小时前，卡托普利并未进一步降低对脊髓刺激的升压反应。相反，沙拉新显著增强了神经源性血管收缩。结果表明，在脊髓麻醉的正常血压大鼠中，卡托普利和沙拉新都通过使血管平滑肌舒张来减弱对脊髓刺激的高血压反应。除了这一共同机制外，还可观察到卡托普利和沙拉新对神经源性血管收缩的不同作用。与沙拉新不同，卡托普利可能通过阻断血管紧张素II（AII）低于升压水平时诱导的交感易化作用来抑制脊髓麻醉的正常血压大鼠的神经源性血管收缩。在脊髓麻醉的正常血压大鼠中，沙拉新可能模拟低于升压水平的AII的交感易化作用。
