Localization of the vasopressin V1a and V2 receptors within the renal cortical and medullary circulation.

Localization of the vasopressin V1a and V2 receptors within the renal cortical and medullary circulation.
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加压素 V1a 和 V2 受体在肾皮质和髓质循环中的定位。

DOI:
10.1152/ajpregu.1997.273.1.r243
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发表时间:
1997
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
CowleyJr,AW
CowleyJr,AW
中科院分区:
--
文献类型:
--
作者:
Park,F;Mattson,DL;Skelton,MM;CowleyJr,AW

文献摘要

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精氨酸加压素(AVP)是一种强有力的血管收缩剂,通过刺激加压素V1 a受体(V1 aR)优先减少肾髓质血流量。研究还表明,加压素V2受体(V2 R)可调节AVP介导的血管收缩。目前,V1 aR和V2 R在肾皮质和髓质微循环中的分布尚未确定。本研究的目的是本地化的V1 aR和V2 R的转录和翻译位点的显微解剖肾内血管段的皮质和髓质,特别是叶间,弓状和小叶间动脉;传入和传出小动脉;肾小球;和单一的外髓直血管毛细血管使用逆转录-聚合酶链反应和蛋白质印迹分析。结果表明,在离体肾皮质和髓质血管中均存在V1 aR的mRNA和蛋白,而未发现V2 R的mRNA和蛋白,提示AVP在肾髓质的缩血管作用是通过V1 aR介导的,而V2 R介导的血管舒张作用可能是通过肾间质或肾小管细胞内的旁分泌激素的释放来调节的。
Arginine vasopressin (AVP) is a potent vasoconstrictor that preferentially reduces renal medullary blood flow through the stimulation of the vasopressin V1a receptor (V1aR). Studies have also shown that the vasopressin V2 receptor (V2R) may modulate AVP-mediated vasoconstriction. At present, the distribution of the V1aR and V2R within the renal cortical and medullary microcirculation has not been determined. This study was designed to localize the transcriptional and translational sites of the V1aR and V2R in microdissected intrarenal vascular segments from both the cortex and medulla, specifically the interlobar, arcuate, and interlobular arteries; afferent and efferent arterioles; glomeruli; and single outer medullary vasa recta capillaries using reverse transcription-polymerase chain reaction and Western blot analyses. The results indicated that V1aR mRNA and proteins were present in the isolated cortical or medullary vasculature, but the V2R mRNA and proteins were not found. This study suggests that the vasoconstrictor action of AVP within the renal medulla is mediated through the V1aR and that the modulatory V2R-mediated vasodilation is probably through the release of paracrine hormones found within the renal interstitial or tubular cells.