Nobiling R, Münter K, Bührle C P, Hackenthal E
Physiologisches Institut, Universität Heidelberg, Federal Republic of Germany.
Pflugers Arch. 1990 Mar;415(6):713-7. doi: 10.1007/BF02584010.
It is well established that renin release from the juxtaglomerular epithelioid cells in the media of the afferent arteriole strongly depends on the mean renal perfusion pressure, whereas a possible influence of the pulsation of blood pressure on renin release has only occasionally been investigated, and the results are contradictory. Such an influence on renin release cannot be excluded because pulsation is known to modulate arterial baroreceptors and vascular tone in some resistance vessels. In the isolated perfused rat kidney, we found a pulsation amplitude-dependent inhibition of renin release that could be blocked either by vasodilatation or by calcium channel blockade. The inhibition occurred at perfusion pressures between 85 and 125 mm Hg. The underlying pulsation pressure-sensitive mechanism has to be ascribed integrating properties, because a constant-flow pressure rise to the "systolic" value of pulsatile perfusion resulted in virtually the same inhibition of renin release. Moreover, a reduced urine flow during pulsatile perfusion provides evidence for preglomerular constriction under these conditions. It is concluded that, besides pathological changes of renal perfusion pressure, variations of the pulse amplitudes, e.g. resulting from renal artery stenosis or atherosclerosis, may also influence renin release and contribute to renovascular hypertension.
众所周知，入球小动脉中膜的球旁上皮样细胞释放肾素强烈依赖于平均肾灌注压，而血压搏动对肾素释放的可能影响仅偶尔被研究，且结果相互矛盾。这种对肾素释放的影响不能排除，因为已知搏动可调节某些阻力血管中的动脉压力感受器和血管张力。在离体灌注的大鼠肾脏中，我们发现肾素释放受到搏动幅度依赖性抑制，这种抑制可通过血管舒张或钙通道阻滞来阻断。抑制作用发生在85至125毫米汞柱的灌注压力下。潜在的搏动压力敏感机制必须归因于整合特性，因为恒定流量压力升至搏动灌注的“收缩期”值会导致肾素释放受到几乎相同的抑制。此外，搏动灌注期间尿量减少为这些条件下的肾前性收缩提供了证据。得出的结论是，除了肾灌注压的病理变化外，例如由肾动脉狭窄或动脉粥样硬化引起的脉搏幅度变化，也可能影响肾素释放并导致肾血管性高血压。
