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卡巴胆碱刺激大鼠下颌下腺碎片中肌醇磷酸积累的作用不受血管活性肠肽的影响。

Carbachol stimulation of inositol phosphate accumulation in rat submandibular gland fragments is not modified by VIP.

作者信息

Larsson O, Fredholm B B

机构信息

Department of Pharmacology, Karolinska Institutet, Stockholm, Sweden.

出版信息

Acta Physiol Scand. 1989 Mar;135(3):263-9. doi: 10.1111/j.1748-1716.1989.tb08576.x.

Abstract

Formation of inositol phosphates in response to carbachol, phenylephrine and vasoactive intestinal polypeptide (VIP) was studied after labelling with [3H]myo-inositol in rat submandibular gland fragments. Carbachol enhanced the accumulation of inositol phosphates in a concentration-dependent manner. This effect was independent of calcium in the incubation medium and totally antagonized by atropine (IC50 = approx. I nM). Phenylephrine also induced an increase in inositol phosphate accumulation, which was totally antagonized by prazosin but not by atropine. Vasoactive intestinal polypeptide, isoproterenol and forskolin, compounds known to enhance the levels of cAMP in rat salivary gland, or addition of dibutyryl-cAMP (DB-cAMP) failed to alter basal or carbachol-evoked accumulation of inositol phosphates. It is concluded that the formation of inositol phosphates during muscarinic receptor stimulation with carbachol in rat submandibular gland fragments is not affected by adrenoceptor occupation or by cAMP. In particular, addition of VIP, which coexists with acetylcholine, did not alter the muscarinic inositol phosphate response.

摘要

用[3H]肌醇标记大鼠下颌下腺碎片后,研究了毒蕈碱、去氧肾上腺素和血管活性肠肽(VIP)刺激下肌醇磷酸的形成。毒蕈碱以浓度依赖的方式增强了肌醇磷酸的积累。这种效应与孵育培养基中的钙无关,且完全被阿托品拮抗(IC50约为1 nM)。去氧肾上腺素也诱导肌醇磷酸积累增加,这完全被哌唑嗪拮抗,但不被阿托品拮抗。血管活性肠肽、异丙肾上腺素和福斯可林(已知可提高大鼠唾液腺中cAMP水平的化合物)或添加二丁酰-cAMP(DB-cAMP)均未改变基础或毒蕈碱诱发的肌醇磷酸积累。结论是,在大鼠下颌下腺碎片中,毒蕈碱受体刺激期间肌醇磷酸的形成不受肾上腺素能受体占据或cAMP的影响。特别是,与乙酰胆碱共存的VIP的添加并未改变毒蕈碱肌醇磷酸反应。

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