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首页> 外文期刊>American Journal of Physiology >Opioid receptor-like 1 stimulation in the collecting duct induces aquaresis through vasopressin-independent aquaporin-2 downregulation.
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Opioid receptor-like 1 stimulation in the collecting duct induces aquaresis through vasopressin-independent aquaporin-2 downregulation.

机译：收集管中的类鸦片受体样1刺激通过不依赖血管加压素的aquaporin-2下调诱导水肿。

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摘要

Nociceptin, the endogenous ligand of the inhibitory G protein-coupled opioid receptor-like 1 receptor, produces aquaresis (i.e., increases the excretion of solute-free urine) in rats. However, the mechanism underlying this effect has not yet been explained. Using immunohistochemistry, we found the opioid receptor-like 1 receptor in the rat kidney colocalized with the vasopressin-regulated water channel aquaporin-2 in inner medullary collecting ducts. We investigated the aquaretic effect of opioid receptor-like 1 receptor stimulation by infusing the selective nociceptin analog ZP120C; volume depletion was prevented by computer-driven, servo-controlled intravenous volume replacement with 50 mM glucose. ZP120C induced a marked and sustained aquaresis in normal and congestive heart failure rats in the absence of changes in vasopressin plasma concentrations. The ZP120C-induced aquaresis was associated with downregulation of the aquaporin-2 protein level in both rat groups, suggesting that opioid receptor-like 1 receptor stimulation produces aquaresis by inhibiting the vasopressin type-2 receptor-mediated stimulation on collecting duct water reabsorption. However, substantial amounts of PKA-mediated serine 256 phosphorylated aquaporin-2 were still present after 4 h of ZP120C treatment. Furthermore, neither preincubation with nociceptin nor ZP120C inhibited vasopressin-mediated cAMP accumulation in isolated collecting ducts. We conclude that renal opioid receptor-like 1 receptor stimulation in normal and congestive heart failure rats produces aquaresis by a direct renal effect, via aquaporin-2 downregulation, through a mechanism not involving inhibition of vasopressin type-2 receptor-mediated cAMP production.
机译：Nociceptin是抑制性G蛋白偶联类阿片受体样1受体的内源性配体，可在大鼠中产生水泡现象（即增加无溶质尿液的排泄）。但是，尚未解释这种作用的机制。使用免疫组织化学，我们在大鼠肾脏中发现了阿片样物质受体样1受体与血管加压素调节的水通道Aquaporin-2在髓内收集管中共定位。我们通过注入选择性伤害感受器类似物ZP120C来研究类阿片受体样1受体刺激的水生生物效应。通过使用50 mM葡萄糖的计算机驱动，伺服控制的静脉内容积置换来防止容积减少。 ZP120C在正常和充血性心力衰竭大鼠中诱导了明显而持续的水肿，而加压素血浆浓度没有变化。 ZP120C诱导的水肿与两组大鼠水通道蛋白2的表达下调有关，这表明类鸦片受体样1受体刺激通过抑制血管加压素2型受体介导的刺激来收集导管水重吸收而产生水肿。但是，ZP120C处理4小时后，仍存在大量PKA介导的丝氨酸256磷酸化aquaporin-2。此外，与Nociceptin或ZP120C的预温育均不能抑制血管加压素介导的cAMP在分离的收集管中的蓄积。我们得出的结论是，正常和充血性心力衰竭大鼠中的肾阿片样受体1受体刺激通过水通道蛋白2下调，通过不涉及抑制2型加压素介导的cAMP产生的机制，通过直接的肾脏作用而产生水肿。

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