Faber J E
Department of Physiology, University of North Carolina, Chapel Hill 27514.
Clin Exp Hypertens A. 1987;9 Suppl 1:241-57. doi: 10.3109/10641968709160177.
We previously identified a sympathoexcitatory pressor reflex that is evoked by acute (90 min) unilateral renal artery stenosis (RST). The reflex is strongly expressed in conscious rats when the renin-angiotensin system and baroreflexes are diminished by captopril and sinoaortic denervation, and is eliminated by denervation of the stenosed kidney. In the present study, dorsal rhizotomy inhibited the reflex, establishing the role of afferent renal nerves (ARN). During sustained (10 h) RST, the reflex reversed within 4 hours after onset of RST, but persisted after removal of the contralateral kidney. Hematocrit measurements did not support pressure diuresis as a mechanism for inhibition by the contralateral kidney. Other studies suggest that ARN signals and/or release of antihypertensive renomedullary lipid from the contralateral kidney are not involved in inhibition of the reflex. These data suggest that the contralateral kidney can oppose, at least acutely by an as yet undefined mechanism, an ARN-dependent pressor reflex evoked by ipsilateral renal artery stenosis.
我们之前发现了一种交感神经兴奋性升压反射,它由急性(90分钟)单侧肾动脉狭窄(RST)诱发。当通过卡托普利和去窦主动脉神经支配使肾素-血管紧张素系统和压力反射减弱时,该反射在清醒大鼠中强烈表达,并且通过对狭窄肾脏去神经支配可消除该反射。在本研究中,背根切断术抑制了该反射,确立了肾传入神经(ARN)的作用。在持续性(10小时)RST期间,该反射在RST开始后4小时内逆转,但在切除对侧肾脏后持续存在。血细胞比容测量结果不支持压力性利尿作为对侧肾脏抑制的一种机制。其他研究表明,ARN信号和/或来自对侧肾脏降压性肾髓质脂质的释放与该反射的抑制无关。这些数据表明,对侧肾脏至少可以通过一种尚未明确的机制,急性对抗由同侧肾动脉狭窄诱发的依赖于ARN的升压反射。