Murray B M
Department of Medicine, SUNY, Buffalo.
Circ Res. 1990 Aug;67(2):440-7. doi: 10.1161/01.res.67.2.440.
Male Sprague-Dawley rats (200-250 g) were fed low protein (6%) diets (LP rats), high protein (50%) diets (HP rats), or regular rat chow (approximately 16% protein) (control rats) and studied under anesthesia after 2 weeks. Dietary protein intake did not affect mean arterial pressure, but renal blood flow was increased in the HP rats and decreased in the LP rats compared with the control rats. Mesenteric blood flow was not significantly different in the three diet groups. Captopril (10 mg.kg-1 i.v.) had no effect on renal vascular resistance in the HP rat but did reduce the elevated renal vascular resistance seen in the LP rat. Meclofenamate (5 mg.kg-1 i.v.) did not significantly affect renal hemodynamics in either HP or LP rats. Finally, the HP rat exhibited resistance to the systemic pressor, renal, and mesenteric vasoconstrictor effects of angiotensin II. Captopril restored the systemic pressor and the mesenteric vasoconstrictor response but not the renal vasoconstrictor response to angiotensin II. Meclofenamate, on the other hand, restored both the systemic pressor response and the renal vasoconstrictor response. Thus, in the LP rat, the vascular response to angiotensin II remains intact, and renal vasoconstriction appears to be mediated by angiotensin II. In contrast, in the HP rat, the renovascular response to angiotensin II is blunted apparently because of enhanced renal prostaglandin production. However, neither increased renal prostaglandin synthesis nor blunting of the renovascular response to angiotensin II appears to account for the chronic vasodilation seen in the HP rat.
将200 - 250克的雄性斯普拉格 - 道利大鼠分为三组，分别喂食低蛋白（6%）饮食（LP大鼠）、高蛋白（50%）饮食（HP大鼠）或常规大鼠饲料（约16%蛋白质）（对照大鼠），2周后在麻醉状态下进行研究。饮食蛋白质摄入量不影响平均动脉压，但与对照大鼠相比，HP大鼠的肾血流量增加，LP大鼠的肾血流量减少。三组饮食组的肠系膜血流量无显著差异。卡托普利（10毫克·千克⁻¹静脉注射）对HP大鼠的肾血管阻力无影响，但可降低LP大鼠升高的肾血管阻力。甲氯芬那酸（5毫克·千克⁻¹静脉注射）对HP或LP大鼠的肾血流动力学均无显著影响。最后，HP大鼠对血管紧张素II的全身升压、肾和肠系膜血管收缩作用表现出抵抗。卡托普利恢复了血管紧张素II的全身升压和肠系膜血管收缩反应，但未恢复肾血管收缩反应。另一方面，甲氯芬那酸恢复了全身升压反应和肾血管收缩反应。因此，在LP大鼠中，对血管紧张素II的血管反应保持完整，肾血管收缩似乎由血管紧张素II介导。相反，在HP大鼠中，对血管紧张素II的肾血管反应明显减弱，显然是由于肾前列腺素生成增加。然而，肾前列腺素合成增加和对血管紧张素II的肾血管反应减弱似乎都不能解释HP大鼠中所见的慢性血管舒张。
