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由不同的血管活性肠肽和蜂毒明肽敏感的垂体腺苷酸环化酶激活肽受体介导的结肠带抑制性传递。

Inhibitory transmission in tenia coli mediated by distinct vasoactive intestinal peptide and apamin-sensitive pituitary adenylate cyclase activating peptide receptors.

作者信息

Jin J G, Katsoulis S, Schmidt W E, Grider J R

机构信息

Department of Physiology, Medical College of Virginia, Richmond.

出版信息

J Pharmacol Exp Ther. 1994 Aug;270(2):433-9.

PMID:8071835
Abstract

Inhibitory transmission in tenia coli involves both vasoactive intestinal peptide (VIP) and an apamin-sensitive transmitter. The present study examined whether pituitary adenylate cyclase activating peptide (PACAP) is released from tenia coli and accounts for the apamin-sensitive component of neurally mediated relaxation. Electrical field stimulation (0.25-4 Hz) elicited frequency-dependent relaxation and PACAP release; earlier studies had shown a similar pattern for VIP release and an absence of nitric oxide generation in this tissue. A combination of specific PACAP-27 and PACAP-38 monoclonal antibodies (each 100 micrograms/ml), the PACAP antagonist PACAP6-38 and desensitization with PACAP inhibited relaxation induced by all frequencies of stimulation. The magnitude of inhibition elicited by each treatment (38 +/- 3%-41 +/- 3% at 4 Hz) was similar to that elicited by apamin (44 +/- 11%) and was not augmented by apamin. VIP antibody (1:60), the VIP antagonist, VIP10-28 and VIP desensitization also inhibited relaxation (33 +/- 2%-35 +/- 5% at 4 Hz). Inhibition by each treatment was augmented additively by apamin (76 +/- 3%-85 +/- 3%) as well as by combination with PACAP antibody, PACAP antagonist and PACAP desensitization (76 +/- 6%-80 +/- 3%). Measurements in muscle strips and dispersed tenia coil muscle cells showed that VIP10-28 inhibited relaxation induced by VIP only, and PACAP6-38 inhibited relaxation mediated by PACAP-27 or PACAP-38 only, implying interaction of VIP and PACAP with distinct receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

结肠带中的抑制性传递涉及血管活性肠肽(VIP)和一种蜂毒明肽敏感的递质。本研究检测了垂体腺苷酸环化酶激活肽(PACAP)是否从结肠带释放,并介导神经介导的舒张中蜂毒明肽敏感成分。电场刺激(0.25 - 4 Hz)引起频率依赖性舒张和PACAP释放;早期研究表明该组织中VIP释放有类似模式且不产生一氧化氮。特异性PACAP - 27和PACAP - 38单克隆抗体(各100微克/毫升)、PACAP拮抗剂PACAP6 - 38以及用PACAP脱敏均可抑制所有刺激频率诱导的舒张。每种处理引起的抑制程度(4 Hz时为38±3% - 41±3%)与蜂毒明肽引起的相似(44±11%),且不被蜂毒明肽增强。VIP抗体(1:60)、VIP拮抗剂VIP10 - 28和VIP脱敏也抑制舒张(4 Hz时为33±2% - 35±5%)。每种处理的抑制作用在与蜂毒明肽联合时(76±3% - 85±3%)以及与PACAP抗体、PACAP拮抗剂和PACAP脱敏联合时(76±6% - 80±3%)呈相加增强。在肌条和分散的结肠带肌细胞中的测量表明,VIP10 - 28仅抑制由VIP诱导的舒张,而PACAP6 - 38仅抑制由PACAP - 27或PACAP - 38介导的舒张,这意味着VIP和PACAP与不同受体相互作用。(摘要截断于250字)

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