Effect of angiotensin II and norepinephrine on isolated rat afferent and efferent arterioles.
Effect of angiotensin II and norepinephrine on isolated rat afferent and efferent arterioles.
复制标题
血管紧张素 II 和去甲肾上腺素对离体大鼠传入和传出小动脉的影响。
DOI：
10.1152/ajprenal.1990.258.3.f741
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Conger,JD
中科院分区：
文献类型：
--
作者：
Yuan,BH;Robinette,JB;Conger,JD
肾小球前动脉和肾小球后动脉对血管紧张素II(Ang II)和去甲肾上腺素(NE)收缩活性的不同敏感性是有争议的。为了避免复杂的血管外神经体液变量在完整的大鼠肾脏上造成不同的结果，我们用一种离体微动脉技术研究了血管紧张素II和去甲肾上腺素在SD大鼠的传入和传出小动脉上的剂量效应。电针对血管紧张素Ⅱ的敏感性高于电针(EC_(50)=3.2+/-1.8×10(-11)和1.0+/-1.6×10(-9)M，P<0.001)，而电针和电针对去甲肾上腺素的敏感性相似(分别为3.4+/-2.3×10(-8)和1.4+/-2.6×10(-8)M)。不同管腔压力(90和30 mm Hg)灌流时，AA对Ang II的量效曲线无明显差异。而在30毫米汞柱时，电针对血管紧张素Ⅱ的敏感性高于90毫米汞柱(分别为3.0+/-1.2×10(-11)和5.0+/-1.8×10(-10)M，P<0.005)。电针对去甲肾上腺素的EC50不受管腔压力类似变化的影响。加入10(-5)M吲哚美辛后，AA对Ang II的平均剂量-反应曲线与未加10(-5)M吲哚美辛时相同，但对Ang II呈局灶性收缩的微动脉，其反应趋于一致。结果表明，在分离的大鼠肾小球小动脉中，电针对Ang II比AA更敏感，但两条血管对NE的反应相似。再障患者Ang II敏感性的降低与体内较高的压力无关，而且AA患者的减弱反应似乎主要不是通过Ang II刺激的血管扩张剂前列腺素活性来调节的。电针对血管紧张素转换酶II的敏感性似乎与管腔压力呈负相关。
Differential sensitivity of the pre- and postglomerular arterial vessels to vasoconstrictor activity of angiotensin II (ANG II) and norepinephrine (NE) is controversial. To avoid the complex extravascular neurohumoral variables that may have accounted for different results in the intact rat kidney, an isolated arteriole technique was used to examine the dose responses of ANG II and NE on afferent (AA) and efferent arterioles (EA) from Sprague-Dawley rats. EA were more sensitive than AA to ANG II (EC50 = 3.2 +/- 1.8 x 10(-11) and 1.0 +/- 1.6 x 10(-9) M, respectively, P less than 0.001), whereas EC50 of both AA and EA to NE were similar (3.4 +/- 2.3 x 10(-8) and 1.4 +/- 2.6 x 10(-8) M, respectively). The dose-response curves of AA to ANG II were not different when perfused at different luminal pressures (90 and 30 mmHg). In contrast, EA were more sensitive to ANG II at 30 than at 90 mmHg (3.0 +/- 1.2 x 10(-11) and 5.0 +/- 1.8 x 10(-10) M, respectively, P less than 0.005). The EC50 of EA to NE was unaffected by similar changes in luminal pressures. The mean dose-response curves of AA to ANG II were the same with and without the addition of 10(-5) M indomethacin; however, in arterioles displaying a focal constriction pattern to ANG II the response became uniform. It is concluded that, in the isolated rat glomerular arterioles, EA are more sensitive to ANG II than AA, but both vessels respond similarly to NE. The decreased ANG II sensitivity in AA is not related to the higher in vivo pressure, and the attenuated response in AA does not appear to be mediated primarily through ANG II-stimulated vasodilator prostanoid activity. EA sensitivity to ANG II appears to be inversely related to lumen pressure.