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血管加压素(AVP)以相反的方式刺激培养的肾小管间质肌成纤维细胞(RIMCT细胞)中的腺苷酸环化酶和磷脂酶C。

AVP stimulates adenylyl cyclase and phospholipase C in reciprocal fashion in cultured RIMCT cells.

作者信息

Teitelbaum I, Strasheim A

机构信息

Department of Medicine, University of Colorado School of Medicine, Denver 80262.

出版信息

Am J Physiol. 1990 Oct;259(4 Pt 1):C693-6. doi: 10.1152/ajpcell.1990.259.4.C693.

Abstract

In cultured rat inner medullary collecting tubule (RIMCT) cells, arginine vasopressin (AVP) stimulates adenylyl cyclase (AC) activity in dose-dependent fashion, with no response at concentrations of 10(-10) M or below and with peak activity at 10(-7) M AVP. In contrast, AVP-stimulated phospholipase (PLC) activity is greatest at concentrations at which there is no effect on AC and decreases at higher concentrations of AVP, becoming undetectable at 10(-7) M. Increasing cellular adenosine 3',5'-cyclic monophosphate (cAMP) content with either exogenous ClPheScAMP or forskolin eliminates inositol trisphosphate production in response to 10(-13) M AVP. Conversely, inhibition of AC by 2',5'-dideoxyadenosine (DDA) unmasks PLC activity in response to 10(-7) M AVP that is not observed in the absence of DDA. Similarly, DDA prevents inhibition of epidermal growth factor-stimulated PLC by AVP. These findings demonstrate the reciprocal relationship between AVP-stimulated AC and PLC activities in cultured RIMCT cells, which may explain previous divergent results regarding the ability of AVP to stimulate PLC in this tissue.

摘要

在培养的大鼠髓质内集合管(RIMCT)细胞中,精氨酸加压素(AVP)以剂量依赖方式刺激腺苷酸环化酶(AC)活性,在10^(-10) M或更低浓度时无反应,在10^(-7) M AVP时活性达到峰值。相反,AVP刺激的磷脂酶(PLC)活性在对AC无影响的浓度下最大,并在更高浓度的AVP时降低,在10^(-7) M时变得无法检测到。用外源性ClPheScAMP或福司可林增加细胞内环磷酸腺苷(cAMP)含量可消除对10^(-13) M AVP的肌醇三磷酸生成反应。相反,2',5'-二脱氧腺苷(DDA)对AC的抑制作用可揭示对10^(-7) M AVP的PLC活性,而在没有DDA的情况下未观察到这种活性。同样,DDA可防止AVP对表皮生长因子刺激的PLC的抑制作用。这些发现证明了培养的RIMCT细胞中AVP刺激的AC和PLC活性之间的相互关系,这可能解释了先前关于AVP刺激该组织中PLC能力的不同结果。

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