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生长抑素抑制激素释放的分子机制:电压门控钙通道和G蛋白的参与

Molecular mechanisms of somatostatin's inhibition of hormone release: participation of voltage-gated calcium channels and G-proteins.

作者信息

Scherübl H, Hescheler J, Riecken E O

机构信息

Department of Gastroenterology, University Hospital Steglitz, Free University of Berlin, Germany.

出版信息

Horm Metab Res Suppl. 1993;27:1-4.

PMID:8101178
Abstract

Somatostatin is known to inhibit hormone release from various neuroendocrine cells. In order to understand the mechanisms underlying somatostatin's action we performed patch-clamp experiments in GH3 pituitary, rMTC 44-2 thyroid and BON carcinoid cells. Calcium-mediated hormone release depended on the intracellular calcium concentration and thus on the calcium influx through voltage-gated calcium channels. In addition to inhibiting the cAMP-dependent secretory pathway, somatostatin reduced the calcium inward currents and thereby hormone release. The inhibition of voltage-gated calcium channels by somatostatin was mediated by "signal transducing" Go proteins. Thus, somatostatin's actions on hormone release involve both cAMP and intracellular calcium as second messengers. Patch-clamp experiments of voltage-gated calcium channels allow functional studies on the coupling of somatostatin receptors to cellular effector systems.

摘要

已知生长抑素可抑制多种神经内分泌细胞释放激素。为了解生长抑素作用的潜在机制,我们在GH3垂体细胞、rMTC 44 - 2甲状腺细胞和BON类癌细胞中进行了膜片钳实验。钙介导的激素释放取决于细胞内钙浓度,因此取决于通过电压门控钙通道的钙内流。除了抑制cAMP依赖性分泌途径外,生长抑素还减少了钙内向电流,从而减少了激素释放。生长抑素对电压门控钙通道的抑制作用是由“信号转导”Go蛋白介导的。因此,生长抑素对激素释放的作用涉及cAMP和细胞内钙作为第二信使。电压门控钙通道的膜片钳实验允许对生长抑素受体与细胞效应系统的偶联进行功能研究。

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