Steele T H
Department of Medicine, University of Wisconsin, Madison.
Am J Nephrol. 1987;7 Suppl 1:17-23. doi: 10.1159/000167538.
In the isolated perfused rat kidney, the superimposition of a number of calcium entry blockers (CEB) upon norepinephrine vasoconstriction prompts an increase in the glomerular filtration rate (GFR) to a level substantially greater than the original value. A similar acute GFR response to CEB is manifested in the intact anesthetized rat with the renal perfusion pressure remaining constant. This glomerular response to CEB is accentuated in isolated perfused kidneys from Dahl salt-sensitive (DS) rats as compared with kidneys from Dahl salt-resistant (DR) rats. The disparities between DS and DR kidney responses are further amplified in the DS rat kidney after a high NaCl intake and the development of hypertension by the DS rat. In addition, vasoconstrictor responses to BAY-K 8644, a calcium entry facilitator, are accentuated in DS rat kidneys, and even more so following a high NaCl intake or 'chemical sympathectomy' with 6-hydroxydopamine. These results suggest that subtle changes in vascular and glomerular calcium entry modulation may be the key determinants of altered renal hemodynamics in salt-dependent hypertension.
在离体灌注的大鼠肾脏中，多种钙通道阻滞剂（CEB）叠加于去甲肾上腺素引起的血管收缩之上，会促使肾小球滤过率（GFR）升高至显著高于初始值的水平。在肾灌注压保持恒定的完整麻醉大鼠中，也表现出对CEB类似的急性GFR反应。与 Dahl 盐抵抗（DR）大鼠的肾脏相比，来自 Dahl 盐敏感（DS）大鼠的离体灌注肾脏中，这种对CEB的肾小球反应更为明显。在DS大鼠摄入高盐并发展为高血压后，DS大鼠肾脏与DR大鼠肾脏反应之间的差异进一步扩大。此外，在DS大鼠肾脏中，对钙通道促进剂BAY-K 8644的血管收缩反应更为明显，在高盐摄入或用6-羟基多巴胺进行“化学交感神经切除术”后更是如此。这些结果表明，血管和肾小球钙内流调节的细微变化可能是盐依赖性高血压中肾血流动力学改变的关键决定因素。
