Guanosine 3',5'-cyclic monophosphate as a mediator of inhibition of renin release.
Guanosine 3',5'-cyclic monophosphate as a mediator of inhibition of renin release.
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鸟苷 3,5-环单磷酸作为抑制肾素释放的介质。
DOI：
10.1152/ajprenal.1988.255.3.f474
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Campbell,WB
中科院分区：
文献类型：
--
作者：
Henrich,WL;McAllister,EA;Smith,PB;Campbell,WB
在两种不同的体外制剂中，检测了鸟苷3 '，5'-环一磷酸（cGMP）作为组织肾素释放抑制介质的作用。在大鼠表层皮层切片中，由异丙肾上腺素（10（-5）M）刺激的肾素释放被心房肽III（ANP，2.1 × 10（-8）M）、硝普钠（NP，10（-3）M）和8-溴鸟苷3 '，5'-环一磷酸（8-BrcGMP，10（-3）和10（-6）M）消除。ANP和8-BrcGMP（10（-3）和10（-6）M）也抑制花生四烯酸（10（-3）M）刺激的肾素释放。ANP和NP均显著增加组织cGMP浓度（P <0.05），但均不影响环磷酸腺苷（cAMP）浓度。当将鸟苷酸环化酶抑制剂亚甲蓝（10（-5）M）加入到与异丙肾上腺素和ANP孵育的切片中时，ANP对肾素释放的抑制作用被消除。这些结果在分离培养的大鼠肾小球细胞的制备中得到证实。在这些细胞中，异丙肾上腺素诱导的肾素释放显着增加（58%，P <0.01），这是由添加8-BrcGMP（10（-6）M）抑制。这些数据表明，ANP对异丙肾上腺素和花生四烯酸诱导的肾素释放的直接抑制作用。NP、8-BrcGMP和亚甲蓝的结果表明cGMP是这种抑制的细胞内介质。
The role of guanosine 3',5'-cyclic monophosphate (cGMP) as an inhibitory mediator of tissue renin release was examined in two different in vitro preparations. In rat superficial cortical slices, renin release stimulated by isoproterenol (10(-5) M) was ablated by atriopeptin III (ANP, 2.1 x 10(-8) M), nitroprusside (NP, 10(-3) M), and 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP, 10(-3) and 10(-6) M). Arachidonic acid (10(-3) M)-stimulated renin release was also inhibited by ANP and 8-BrcGMP (10(-3) and 10(-6) M). Both ANP and NP increased tissue cGMP concentrations significantly (P less than 0.05), but neither had an effect on adenosine 3',5'-cyclic monophosphate (cAMP) concentrations. When methylene blue (10(-5) M), an inhibitor of guanylate cyclase, was added to slices incubated with isoproterenol and ANP, the inhibition of renin release by ANP was abolished. These results were confirmed in a preparation of isolated cultured rat juxtaglomerular cells. In these cells, isoproterenol induced a significant increase (58%, P less than 0.01) in renin release, which was inhibited by the addition of 8-BrcGMP (10(-6) M). These data demonstrate a direct inhibitory effect of ANP on isoproterenol- and arachidonic acid-induced renin release. The results with NP, 8-BrcGMP, and methylene blue suggest that cGMP is an intracellular mediator of this inhibition.