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单肾单夹型 Goldblatt 高血压大鼠体内小动脉对去甲肾上腺素和钙的反应性

In vivo arteriolar reactivity to norepinephrine and calcium in one-kidney, one-clip Goldblatt hypertensive rats.

作者信息

Joshua I G, Miller F N, Dowe J P

机构信息

Department of Physiology and Biophysics, School of Medicine, University of Louisville, Kentucky 40292.

出版信息

Clin Exp Hypertens A. 1987;9(11):1691-711. doi: 10.3109/10641968709158967.

DOI:10.3109/10641968709158967
PMID:3436072
Abstract

The in vivo reactivity of small arterioles to norepinephrine and to changes in external calcium was investigated in normotensive (NT) and one-kidney, one-clip Goldblatt hypertensive rats (1K1C). Rats were anesthetized with sodium pentobarbital (50 mg/kg) and arterioles in the cremaster muscle were exposed to increasing concentrations of either norepinephrine (10(-10) to 10(-5) M) or of bath calcium (0 to 5.1 mM). Third-order arterioles of 1K1C showed almost a ten-fold increased reactivity to NE compared to arterioles of NT rats (pD2 values of 7.88 +/- .43 vs 6.92 +/- .30). Arterioles of 1K1C rats showed an increased reactivity to re-exposure to calcium (0.65 to 5.10 mM). Following exposure to phentolamine this hyper-reactivity was abolished and arterioles of 1K1C and NT exhibited similar responses to changes in bath calcium concentrations, suggesting that the increased reactivity in the 1K1C was due to stimulation of endogenous norepinephrine release. When arterioles were exposed to increasing bath concentrations of the calcium entry blockers, verapamil and diltiazem, dilator responses were similar for 1K1C and NT groups. Collectively, these data suggest that during the development of renovascular hypertension, observed increases in arteriolar reactivity involve an increase in the receptor mediated entry of extracellular calcium into vascular smooth muscle and no change in non-receptor-mediated entry of calcium.

摘要

在正常血压(NT)大鼠和单肾单夹Goldblatt高血压大鼠(1K1C)中,研究了小动脉对去甲肾上腺素和细胞外钙变化的体内反应性。用戊巴比妥钠(50mg/kg)麻醉大鼠,将提睾肌中的小动脉暴露于去甲肾上腺素(10⁻¹⁰至10⁻⁵M)或浴钙(0至5.1mM)浓度增加的环境中。与NT大鼠的小动脉相比,1K1C大鼠的三级小动脉对去甲肾上腺素的反应性几乎增加了十倍(pD2值分别为7.88±0.43和6.92±0.30)。1K1C大鼠的小动脉对再次暴露于钙(0.65至5.10mM)表现出更高的反应性。在暴露于酚妥拉明后,这种高反应性被消除,1K1C和NT大鼠的小动脉对浴钙浓度变化表现出相似的反应,这表明1K1C大鼠反应性增加是由于内源性去甲肾上腺素释放受到刺激。当小动脉暴露于钙通道阻滞剂维拉帕米和地尔硫䓬的浴液浓度增加时,1K1C组和NT组的舒张反应相似。总体而言,这些数据表明,在肾血管性高血压的发展过程中,观察到的小动脉反应性增加涉及受体介导的细胞外钙进入血管平滑肌的增加,而非受体介导的钙进入没有变化。

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