Normalization of pressure-natriuresis by nisoldipine in spontaneously hypertensive rats.
Normalization of pressure-natriuresis by nisoldipine in spontaneously hypertensive rats.
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DOI：
10.1161/01.hyp.19.1.49
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发表时间：
1992
期刊：
影响因子：
8.3
通讯作者：
F. Fenoy;M. Kauker;Ivan Milicic;Richard J. Roman
中科院分区：
文献类型：
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作者：
F. Fenoy;M. Kauker;Ivan Milicic;Richard J. Roman
本研究检验了钙拮抗剂尼索地平是否可以使自发性高血压大鼠的钠排泄、乳头血流量、肾间质压和肾灌注压之间的关系转向较低的压力。 Wistar-Kyoto 大鼠和自发性高血压大鼠在服用尼索地平（0.5 微克/千克推注 + 0.017 微克/千克/分钟）后，平均动脉压同样降低了 9% 和 12%。 Wistar-Kyoto 大鼠服用尼索地平后，尿流量和钠排泄分别增加了 35% 和 24%。相比之下，自发性高血压大鼠的尿流量和钠排泄量分别增加了 121% 和 132%，钠排泄分数从 1.9 +/- 0.3 升至 4.2 +/- 0.4%。在相似的肾灌注压下进行比较时，自发性高血压大鼠的控制钠排泄、乳头血流量和肾间质压力显着低于 Wistar-Kyoto 大鼠。自发性高血压大鼠服用尼索地平后，钠排泄、乳头血流量和肾间质压均增加，而对 Wistar-Kyoto 大鼠的乳头血流量或肾间质压没有影响。在给予尼索地平的自发性高血压大鼠中，钠排泄、乳头血流量、肾间质压和肾灌注压之间的关系向较低压力方向转变，并且与 Wistar-Kyoto 大鼠中观察到的相似。这些结果表明，尼索地平使自发性高血压大鼠的钠排泄、肾间质压、乳头血流量和肾灌注压之间的关系正常化，这可能是通过纠正与高血压模型中压力尿钠排泄重置相关的肾髓质灌注缺陷来实现的。
This study examined whether the calcium antagonist nisoldipine can shift the relations between sodium excretion, papillary blood flow, renal interstitial pressure, and renal perfusion pressure toward lower pressures in spontaneously hypertensive rats. Mean arterial pressure decreased similarly by 9% and 12% in Wistar-Kyoto and spontaneously hypertensive rats after nisoldipine (0.5 microgram/kg bolus + 0.017 microgram/kg/min). Urine flow and sodium excretion increased by 35% and 24% in Wistar-Kyoto rats after nisoldipine. In contrast, urine flow and sodium excretion rose by 121% and 132% in spontaneously hypertensive rats, and fractional sodium excretion rose from 1.9 +/- 0.3 to 4.2 +/- 0.4%. Control sodium excretion, papillary blood flow, and renal interstitial pressure were significantly lower in spontaneously hypertensive rats than in Wistar-Kyoto rats when compared at similar renal perfusion pressures. Sodium excretion, papillary blood flow, and renal interstitial pressure all increased in spontaneously hypertensive rats after nisoldipine, whereas it had no effect on papillary blood flow or renal interstitial pressure in Wistar-Kyoto rats. The relations among sodium excretion, papillary blood flow, renal interstitial pressure, and renal perfusion pressure were shifted toward lower pressures in spontaneously hypertensive rats given nisoldipine and became similar to those seen in Wistar-Kyoto rats. These results indicate that nisoldipine normalizes the relations among sodium excretion, renal interstitial pressure, papillary blood flow, and renal perfusion pressure in spontaneously hypertensive rats perhaps by correcting the defect in renal medullary perfusion associated with resetting of pressure natriuresis in this model of hypertension.