腺苷受体激动剂对肾血管的影响。

Renal physiology Pub Date : 1987-01-01 DOI:10.1159/000173135
F G Holz, M Steinhausen
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引用次数: 75

摘要

本实验的目的是确定腺苷激动剂n -乙基-羧酰胺腺苷(NECA), n6 -环己基腺苷(CHA)和2-氯腺苷(2-CLA)对肾血管的影响。用活体电视显微镜观察了失动素麻醉大鼠肾裂肾肾小球前后血管直径的变化。所有代谢稳定的腺苷激动剂局部应用于肾组织浴。NECA是一种优先的A2腺苷受体激动剂,除了对肾小球附近的传入小动脉有小的收缩作用外,还能诱导剂量依赖性的肾小球前和轻微的肾小球后血管舒张。选择性A1腺苷受体激动剂CHA的应用导致所有肾小球前血管收缩,其程度在传入小动脉的最远段最大。2-CLA是一种非选择性激动剂,在所有肾小球前血管中产生小直径减小,肾小球附近的传入小动脉明显收缩,肾小球后血管轻微扩张。NECA增加肾小球血流量,CHA和2-CLA降低肾小球血流量。CHA降低GBF的作用大于2-CLA。从这些实验中可以得出结论,肾脏中存在血管A1和A2腺苷受体,并且A1受体的激活仅与肾小球前血管收缩有关,而A2受体的激活介导肾小球前和肾小球后血管扩张,而远端传入小动脉缺乏血管扩张反应。此外,这些数据表明,这两种受体亚类的非选择性占据与传入小动脉的明显血管收缩和传出小动脉的小血管扩张有关。
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Renovascular effects of adenosine receptor agonists.

The purpose of the present experiments was to determine the renovascular effects of the adenosine agonists N-ethyl-carboxamide adenosine (NECA), N6-cyclohexyl adenosine (CHA) and 2-chloro adenosine (2-CLA). The diameter of pre- and postglomerular vessels in the split hydronephrotic kidney of Inactin-anesthetized rats was measured by in vivo television microscopy. All metabolically stable adenosine agonists were topically applied into the renal tissue bath. NECA, a preferential A2 adenosine receptor agonist, induced dose-dependent marked pre- and slight postglomerular vasodilation except for a small constrictory effect on the afferent arteriole near the glomerulus. Application of CHA, a selective A1 adenosine receptor agonist, led to a vasoconstriction of all preglomerular vessels, the extent of which was greatest at the most distal segment of the afferent arteriole. 2-CLA, a nonselective agonist, produced a small decrease in diameter in all preglomerular vessels, a marked constriction of the afferent arteriole at sites near the glomerulus, and a slight dilation of postglomerular vessels. Glomerular blood flow (GBF) was increased by NECA, and decreased by CHA and 2-CLA. The effects of CHA in reducing GBF were greater than those of 2-CLA. From these experiments it is concluded that vascular A1 and A2 adenosine receptors are present in the kidney and that activation of A1 receptors is associated with preglomerular vasoconstriction only, whereas activation of A2 receptors mediates pre- and postglomerular vasodilation with a lack of vasodilatory response of the distal afferent arteriole. Furthermore, these data indicate that nonselective occupation of both receptor subclasses is associated with marked vasoconstriction of the afferent arteriole and little vasodilation of the efferent arteriole.

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