Endothelium modulates renal blood flow but not autoregulation.
Endothelium modulates renal blood flow but not autoregulation.
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内皮调节肾血流量，但不调节自身调节。
DOI：
10.1152/ajprenal.1992.262.6.f943
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Carretero,OA
中科院分区：
文献类型：
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作者：
Beierwaltes,WH;Sigmon,DH;Carretero,OA
用N-奥米伽-硝基-L-精氨酸甲酯(L-NAME)抑制内皮衍生松弛因子一氧化氮的产生，可使血压升高，肾血流量减少，提示基础内皮松弛因子对全身阻力和肾脏血流均有调节作用。我们检测了L-NAME抑制内皮细胞因子是否也能改变RBF的自我调节。测定去肌动蛋白麻醉SD大鼠的血压和RBF。L-NAME 10 mg/kg体重可产生最大升压反应(23+/-3 mm Hg)，并阻断乙酰胆碱引起的肾血管扩张。对照组大鼠肾灌注压的连续变化表明，RBF自动调节良好，降至95+/-2毫米汞。L-NAME使血压升高，RBF值降低33%(P<0.005)，肾血管阻力增加一倍。虽然RBF减少，但肾脏仍然能够自动调节RBF，尽管在较低的血流附近重置。颈动脉结扎和迷走神经切断术引起的急性高血压使血压升高26+/-6毫米汞柱(P<0.005)，RBF略有增加，但维持自我调节。对L-NAME的升压反应放大至38+/-6毫米汞柱(P<0.001)，但RBF下降35%(P<0.01)。RBF的自动调节保持不变，但在较低流量附近重置。我们的结论是，尽管内皮细胞EDRF的产生可能有助于维持RBF，但它似乎并不介导肾血管对肾灌流压力改变的内在自我调节反应。
Inhibition of the production of the endothelium-derived relaxing factor (EDRF) nitric oxide using N omega-nitro-L-arginine methyl ester (L-NAME) increases blood pressure (BP) and decreases renal blood flow (RBF), suggesting that basal EDRF can modulate both systemic resistance and renal perfusion. We tested whether L-NAME inhibition of EDRF could also change the autoregulation of RBF. Blood pressure and RBF were measured in Inactin-anesthetized Sprague-Dawley rats. A bolus of 10 mg/kg body wt of L-NAME produced the maximum pressor response (23 +/- 3 mmHg) and blocked acetylcholine-induced renal vasodilation. In control rats, sequential changes in renal perfusion pressure showed that RBF was well autoregulated down to 95 +/- 2 mmHg. L-NAME increased BP, decreased RBF by 33% (P less than 0.005), and increased renal vascular resistance twofold. Although RBF was decreased, the kidney was still able to autoregulate RBF, although reset around the lower flow. Acute hypertension by carotid occlusion and vagotomy increased BP by 26 +/- 6 mmHg (P less than 0.005) and slightly increased RBF, while autoregulation was maintained. The pressor response to L-NAME was amplified to 38 +/- 6 mmHg (P less than 0.001), but RBF decreased by 35% (P less than 0.01). Autoregulation of RBF was maintained, although reset around the lower flow. We conclude that, although endothelial EDRF production may help maintain RBF, it does not seem to mediate the intrinsic autoregulatory responses of the renal vasculature to altered renal perfusion pressure.