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首页> 外文期刊>American Journal of Physiology >Adrenergic regulation of salt and fluid secretion in human medullary collecting duct cells.
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Adrenergic regulation of salt and fluid secretion in human medullary collecting duct cells.

机译：肾上腺素调节人类髓质收集导管细胞中的盐和液体分泌。

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摘要

Transepithelial salt and fluid secretion mediated by cAMP in initial inner medullary collecting ducts (IMCDi) may be important for making final adjustments to urine composition. We examined in primary cultures of human IMCDi cells the effects of adrenergic receptor (AR) agonists and antagonists on intracellular cAMP levels, short-circuit current (I(SC)), and fluid secretion. Epinephrine (1 microM), norepinephrine (1 microM), and isoproterenol (10 nM) individually increased intracellular cAMP levels 57-, 2-, and 25-fold, respectively, and stimulated I(SC) 3.3-, 2.9-, and 3.4-fold, respectively. beta-AR activation increased net fluid secretion by cultured human IMCDi cell monolayers from 0.09 +/- 0.04 to 0.26 +/- 0.05 microl x h(-1) x cm(-2) and freshly isolated rat IMCDi from 0.02 +/- 0.01 to 0.09 +/- 0.02 nl x h(-1) x mm(-1). In monolayers, these effects were eliminated by blocking beta2-AR, but not beta1-AR. Activation of alpha2-AR with guanabenz inhibited isoproterenol-induced I(SC) by 37% in human IMCDi monolayers and fluid secretion by 91% in rat IMCDi. Immunohistochemistry of human medullary tissue sections revealed greater expression of beta2-AR than beta1-AR; beta2-AR was localized to the basolateral membranes of human IMCDi. Immunoblots identified alpha2A-AR and alpha2B-AR in cultured human IMCDi cell monolayers. We conclude that 1) catecholamines stimulate cAMP-dependent anion and fluid secretion by IMCDi cells primarily through beta2-AR activation and 2) alpha2-AR activation attenuates cAMP-dependent anion secretion.
机译：由cAMP介导的初始内髓收集管（IMCDi）中的上皮盐和液体分泌对于最终调整尿液成分可能很重要。我们在人IMCDi细胞的原代培养中检查了肾上腺素能受体（AR）激动剂和拮抗剂对细胞内cAMP水平，短路电流（I（SC））和液体分泌的影响。肾上腺素（1 microM），去甲肾上腺素（1 microM）和异丙肾上腺素（10 nM）分别分别提高细胞内cAMP水平57-，2-和25-倍，并刺激I（SC）3.3-，2.9-和3.4折。 β-AR激活使培养的人IMCDi细胞单层的净液分泌从0.09 +/- 0.04增加到0.26 +/- 0.05 microl xh（-1）x cm（-2），新鲜分离的大鼠IMCDi从0.02 +/- 0.01增加到0.09 +/- 0.02 nl xh（-1）x mm（-1）。在单分子层中，这些作用通过阻断beta2-AR而不是beta1-AR消除。胍基苯对α2-AR的激活在人IMCDi单层中抑制了异丙肾上腺素诱导的I（SC）37％，在大鼠IMCDi中抑制了91％的液体分泌。人类髓质组织切片的免疫组织化学显示，β2-AR的表达高于β1-AR。 beta2-AR定位于人IMCDi的基底外侧膜。免疫印迹在培养的人IMCDi细胞单层中鉴定出alpha2A-AR和alpha2B-AR。我们得出的结论是：1）儿茶酚胺主要通过β2-AR激活刺激IMCDi细胞的cAMP依赖性阴离子和液体分泌，2）α2-AR激活减弱cAMP依赖性阴离子的分泌。

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