Lin H B, Young D B
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.
Hypertension. 1988 Jun;11(6 Pt 2):639-44. doi: 10.1161/01.hyp.11.6.639.
The renal hemodynamic and renin release responses to verapamil were analyzed to determine if the antihypertensive action of the calcium entry blocker could be due to its renal effects. Hemodynamic and renin release measurements were compared in a control group of nine anesthetized rabbits and in a group of 10 rabbits given verapamil (200 micrograms/kg i.v. initially, 4 micrograms/kg/min thereafter), starting 30 minutes before data collection. Measurements were made over a range of controlled renal perfusion pressure from 100 to 40 mm Hg. The renal blood flow at 100 mm Hg of the verapamil-treated group was 18% greater (p less than 0.02) than that of the control group, while the glomerular filtration rate was 51% greater (p less than 0.001) than that of the control group. Renal blood flow and glomerular filtration rate autoregulation were highly effective in the control group down to 80 mm Hg, but both variables were poorly regulated in the verapamil-treated group. The filtration fraction of the treated group was 36.9 +/- 1.5% versus 28.5 +/- 1.6% in the control group (p less than 0.003) at 100 mm Hg, and the filtration fraction of the treated group remained significantly greater down to 40 mm Hg. Renin release rates of the two groups were similar at the 100 mm Hg pressure level, but the increase in release due to the progressive reduction in perfusion pressure was significantly greater in the treated group than in the control group. At the 80 mm Hg pressure level, the mean release rate for the treated group was more than three times greater (p less than 0.05) than that of the control group. These findings demonstrate that verapamil is an effective renal vasodilator and that the effect is proportionally greater on the preglomerular than on the postglomerular resistance. This action could be the basis for its antihypertensive efficacy.
分析了维拉帕米对肾血流动力学和肾素释放的反应，以确定钙通道阻滞剂的降压作用是否归因于其对肾脏的影响。在一组9只麻醉兔的对照组和一组10只给予维拉帕米（初始静脉注射200微克/千克，此后4微克/千克/分钟）的兔中比较了血流动力学和肾素释放测量值，在数据收集前30分钟开始给药。在100至40毫米汞柱的一系列可控肾灌注压范围内进行测量。维拉帕米治疗组在100毫米汞柱时的肾血流量比对照组高18%（p<0.02），而肾小球滤过率比对照组高51%（p<0.001）。在对照组中，肾血流量和肾小球滤过率自身调节在降至80毫米汞柱时非常有效，但在维拉帕米治疗组中这两个变量的调节都很差。治疗组在100毫米汞柱时的滤过分数为36.9±1.5%，而对照组为28.5±1.6%（p<0.003），并且治疗组的滤过分数在降至40毫米汞柱时仍显著更高。两组在100毫米汞柱压力水平时的肾素释放率相似，但由于灌注压逐渐降低导致的释放增加在治疗组中比对照组显著更大。在80毫米汞柱压力水平时，治疗组的平均释放率比对照组高三倍多（p<0.05）。这些发现表明维拉帕米是一种有效的肾血管扩张剂，并且该作用对肾小球前阻力的影响比对肾小球后阻力的影响成比例地更大。这种作用可能是其降压疗效的基础。
