Anderson W P, Kline R L, Woods R L
Am J Physiol. 1985 Nov;249(5 Pt 2):H956-67. doi: 10.1152/ajpheart.1985.249.5.H956.
The acute effects of unilateral renal arterial stenosis on systemic and renal hemodynamics were studied in chronically instrumented, conscious dogs. Graded stenosis of one renal artery for 90 min produced graded increases in arterial blood pressure and plasma renin activity and falls in contralateral renal blood flow and total peripheral conductance. There were no significant changes in cardiac output. The changes were transient after mild or moderate renal arterial stenosis but were sustained after severe stenosis. Pentolinium treatment did not significantly affect the hypertension or contralateral renal vasoconstriction caused by moderate or severe renal arterial stenosis. This indicates that the autonomic nervous system did not play a major role in the response to stenosis. In contrast, teprotide abolished the increases in arterial pressure, the contralateral renal vasoconstriction, and the fall in total peripheral conductance in response to stenosis. Thus the acute hypertension following unilateral renal arterial stenosis was due to a decrease in total peripheral conductance caused by decreased conductance of the stenotic kidney due to the stenosis itself (about 20%); vasoconstriction of the contralateral kidney (about 20%), and vasoconstriction of other systemic vasculature (about 60%). The results suggest that angiotensin II was responsible for the vasoconstriction of both the contralateral kidney and the other systemic vasculature.
在长期植入监测装置的清醒犬中,研究了单侧肾动脉狭窄对全身和肾脏血流动力学的急性影响。对一侧肾动脉进行分级狭窄90分钟,会使动脉血压和血浆肾素活性分级升高,对侧肾血流量和总外周血管传导率降低。心输出量无显著变化。轻度或中度肾动脉狭窄后,这些变化是短暂的,但重度狭窄后则持续存在。潘托铵治疗对中度或重度肾动脉狭窄引起的高血压或对侧肾血管收缩无显著影响。这表明自主神经系统在对狭窄的反应中未起主要作用。相反,替普罗肽消除了因狭窄引起的动脉压升高、对侧肾血管收缩以及总外周血管传导率降低。因此,单侧肾动脉狭窄后的急性高血压是由于狭窄本身导致狭窄肾的血管传导率降低(约20%)、对侧肾血管收缩(约20%)以及其他全身血管收缩(约60%)引起的总外周血管传导率降低所致。结果表明,血管紧张素II是对侧肾和其他全身血管收缩的原因。