Ashton N, Swift F V
Faculty of Medicine, Memorial University of Newfoundland, Canada.
Acta Physiol Scand. 1996 Nov;158(3):233-40. doi: 10.1046/j.1365-201X.1996.562312000.x.
Stimulation of the afferent renal nerves in the anaesthetized rabbit by acute reduction in renal perfusion pressure results in a neurally mediated, reflex increase in hindlimb vascular resistance. To determine whether exogenous angiotensin II moderates the reflex, the kidneys of anaesthetized rabbits were vascularly isolated and renal blood flow was occluded acutely, following intrarenal administration of vehicle (0.9% saline) or angiotensin II (0.5 ng), and the hindlimb vascular response was measured. Occlusion of renal blood flow resulted in similar, significant increases in femoral perfusion pressure of 39.7 +/- 7.1 mmHg after vehicle and 21.3 +/- 8.9 mmHg (P < 0.05, n = 6) after angiotensin II. The viability of the preparation following repeated episodes of renal blood flow occlusion was tested by a series of three rapid (2-3 min delay) occlusions and three delayed (30 min delay) occlusions. Femoral perfusion pressure rose by 43.1 +/- 10.7 mmHg (rapid, P < 0.05, n = 11) and 64.4 +/- 12.3 mmHg (delayed, P < 0.05, n = 5) on the first occasion. On the second occasion, the rapid occlusion did not result in a significant increase in femoral perfusion pressure (29.1 +/- 8.1 mmHg), but the delayed group did (54.6 +/- 22.4 mmHg, P < 0.05). On the third occasion, neither group showed a significant change (20.9 +/- 16.3 and 30.8 +/- 13.5 mmHg). These data suggest that exogenous angiotensin II does not moderate the afferent renal nerve reflex. The decline in hindlimb response following rapid serial occlusion may be attributed to a diminution of an intermediary substance(s) at the nerve receptor site.
在麻醉兔中，通过急性降低肾灌注压刺激肾传入神经，会导致神经介导的后肢血管阻力反射性增加。为了确定外源性血管紧张素II是否会调节该反射，对麻醉兔的肾脏进行血管分离，并在肾内注射溶媒（0.9%生理盐水）或血管紧张素II（0.5 ng）后急性阻断肾血流，然后测量后肢血管反应。阻断肾血流后，注射溶媒组股动脉灌注压显著升高39.7±7.1 mmHg，注射血管紧张素II组为21.3±8.9 mmHg（P<0.05，n = 6）。通过一系列三次快速（延迟2 - 3分钟）阻断和三次延迟（延迟30分钟）阻断来测试重复肾血流阻断后标本的活力。第一次时，股动脉灌注压快速阻断时升高43.1±10.7 mmHg（P<0.05，n = 11），延迟阻断时升高64.4±12.3 mmHg（P<0.05，n = 5）。第二次时，快速阻断未导致股动脉灌注压显著升高（29.1±8.1 mmHg），但延迟阻断组升高（54.6±22.4 mmHg，P<0.05）。第三次时，两组均未显示出显著变化（20.9±16.3和30.8±13.5 mmHg）。这些数据表明外源性血管紧张素II不会调节肾传入神经反射。快速连续阻断后后肢反应的下降可能归因于神经受体部位中间物质的减少。
