Steele T H, Challoner-Hue L
Kidney Int. 1987 Apr;31(4):941-5. doi: 10.1038/ki.1987.90.
We studied the responses of isolated perfused kidneys from prehypertensive, salt-sensitive (DS) and salt-resistant (DR) Dahl rats to nitrendipine or verapamil, after norepinephrine vasoconstriction. The perfusion pressure was kept constant. Superimposition of these calcium antagonists upon norepinephrine increased DS GFR by 155% and DR GFR by 58% (P = 0.03), with verapamil increasing the GFR more than nitrendipine (P = 0.02). Nitrendipine and verapamil also partially reversed norepinephrine induced increases in renal vascular resistance, but did not decrease vascular resistance or increase GFR in the absence of norepinephrine. During the increase in GFR produced by calcium antagonists, DR sodium excretion increased, but DS sodium excretion did not. Therefore, calcium antagonists disproportionately increased DS kidney GFR but did not correct DS kidney sodium retention. These data raise the possibility that the DS rat kidney possesses an abnormality of cell calcium regulation affecting glomerular dynamics, and provide evidence that the renal perfusion pressure is more critical than the GFR in adjusting DS rat sodium-excretion.
我们研究了高血压前期、盐敏感（DS）和盐抵抗（DR）Dahl大鼠的离体灌注肾在去甲肾上腺素血管收缩后对尼群地平或维拉帕米的反应。灌注压力保持恒定。这些钙拮抗剂叠加在去甲肾上腺素上使DS组肾小球滤过率（GFR）增加了155%，DR组增加了58%（P = 0.03），维拉帕米使GFR的增加幅度大于尼群地平（P = 0.02）。尼群地平和维拉帕米也部分逆转了去甲肾上腺素引起的肾血管阻力增加，但在没有去甲肾上腺素的情况下，它们并未降低血管阻力或增加GFR。在钙拮抗剂使GFR增加的过程中，DR组的钠排泄增加，但DS组的钠排泄没有增加。因此，钙拮抗剂使DS组肾脏GFR不成比例地增加，但并未纠正DS组肾脏的钠潴留。这些数据增加了DS大鼠肾脏存在影响肾小球动力学的细胞钙调节异常的可能性，并提供了证据表明在调节DS大鼠钠排泄方面，肾灌注压力比GFR更关键。
