Vasopressin V1 receptors on the principal cells of the rabbit cortical collecting tubule. Stimulation of cytosolic free calcium and inositol phosphate production via coupling to a pertussis toxin substrate.
Vasopressin V1 receptors on the principal cells of the rabbit cortical collecting tubule. Stimulation of cytosolic free calcium and inositol phosphate production via coupling to a pertussis toxin substrate.
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兔皮质集合管主细胞上的加压素 V1 受体。
DOI：
10.1172/jci113888
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Spielman,WS
中科院分区：
文献类型：
--
作者：
Burnatowska-Hledin,MA;Spielman,WS
采用荧光Ca2+指示剂fura-2和indo-1检测精氨酸抗利尿素（AVP）对新鲜免疫解剖兔皮质集小管细胞胞浆游离钙浓度（[Ca2+]f）的影响。在细胞悬液中添加AVP可导致[Ca2+]f的快速和短暂增加。1-脱氨基-8- d -AVP （dDVP）是AVP的V2受体激动剂，刺激这些细胞中腺苷3',5' cAMP的产生，对[Ca2+]f没有影响，也不影响AVP诱导的[Ca2+]f的增加。avp诱导的[Ca2+]f升高而非cAMP生成被V1受体拮抗剂[1-（β -巯基- β - β -环五亚甲基丙酸），2-（o-甲基）酪氨酸]arg8 -加压素阻断。avp刺激的[Ca2+]f的增加似乎主要是由于细胞内储存的Ca2+释放，因为EGTA减少细胞外Ca2+对avp诱导的[Ca2+]f的增加几乎没有影响。avp诱导的[Ca2+]f的增加与肌醇1,4,5-三磷酸产生的增加有关，并且似乎涉及鸟嘌呤核苷酸结合蛋白(G)，因为百日咳毒素预处理细胞4-6小时抑制了这种作用。最后，单细胞中[Ca2+]f的测量表明，只有收集小管的主要细胞对AVP的[Ca2+]f的增加有反应。总之，这些结果表明皮质收集小管的主要细胞具有两种不同的抗利尿激素受体系统，众所周知的与腺苷酸环化酶偶联的V2受体，以及导致胞质钙动员的V1受体系统，通过百日咳毒素底物（G蛋白）偶联以产生肌醇磷酸。
The effects of arginine vasopressin (AVP) on the cytosolic free calcium concentration ([Ca2+]f) were examined in freshly immunodissected rabbit cortical collecting tubule cells using fluorescent Ca2+ indicators fura-2 and indo-1. The addition of AVP to a cell suspension resulted in a rapid and transient increase in the [Ca2+]f. The 1-deamino-8-D-AVP (dDVP), a V2 receptor agonist of AVP that stimulated adenosine 3',5' cAMP production in these cells, had no effect on [Ca2+]f and did not affect AVP-induced increase in [Ca2+]f. The AVP-induced increase in [Ca2+]f but not cAMP production was blocked by the V1 receptor antagonist, [1-(beta-mercapto-beta-beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine] Arg8-vasopressin. The AVP-stimulated increase in [Ca2+]f appeared to be largely due to Ca2+ release from intracellular stores as reduction of extracellular Ca2+ with EGTA had little if any effect on the AVP-induced increase in [Ca2+]f. This AVP-induced increase in [Ca2+]f was associated with an increase in inositol-1,4,5-trisphosphate production and appeared to involve a guanine nucleotide-binding protein (G), since the pretreatment of cells with pertussis toxin for 4-6 h inhibited this effect. Finally, measurements of [Ca2+]f in single cells suggest that only the principal cells of the collecting tubules respond to AVP with an increase in [Ca2+]f. In summary, these results demonstrate that the principal cells of the cortical collecting tubule possess two distinct receptor systems for vasopressin, the well-known V2 receptor coupled to adenylate cyclase, and a V1 receptor system that leads to the mobilization of cytosolic calcium, coupled through a pertussis toxin substrate (G protein) to a production of inositol phosphates.