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松弛素对小鼠胃底神经诱导的松弛反应的影响。

Influence of relaxin on the neurally induced relaxant responses of the mouse gastric fundus.

作者信息

Baccari Maria Caterina, Bani Daniele, Bigazzi Mario, Calamai Franco

机构信息

Department of Physiological Sciences, University of Florence, Florence, Italy.

出版信息

Biol Reprod. 2004 Oct;71(4):1325-9. doi: 10.1095/biolreprod.104.029579. Epub 2004 Jun 23.

DOI:10.1095/biolreprod.104.029579
PMID:15215200
Abstract

The peptide hormone relaxin has been reported to depress the amplitude of contractile responses in the mouse gastric fundus by upregulating nitric oxide (NO) biosynthesis at the neural level. In the present study, we investigated whether relaxin also influenced nonadrenergic, noncholinergic (NANC) gastric relaxant responses in mice. Female mice in proestrus or estrus were treated for 18 h with relaxin (1 microg s.c.) or vehicle (controls). Mechanical responses of gastric fundal strips were recorded via force-displacement transducers. In carbachol precontracted strips from control mice and in the presence of guanethidine, electrical field stimulation (EFS) elicited fast relaxant responses that may be followed by a sustained relaxation. All relaxant responses were abolished by tetrodotoxin. Relaxin increased the amplitude of the EFS-induced fast relaxation without affecting either the sustained one or the direct smooth muscle response to papaverine. In the presence of the NO synthesis inhibitor L-N(G)-nitro arginine (L-NNA), that abolished the EFS-induced fast relaxation without influencing the sustained one, relaxin was ineffective. In strips from relaxin-pretreated mice, EFS-induced fast relaxations were enhanced in amplitude with respect to the controls, while sustained ones as well as direct smooth muscle responses to papaverine were not changed. Further addition of relaxin to the bath medium did not influence neurally induced fast relaxant responses, whereas L-NNA did. In conclusion, in the mouse gastric fundus, relaxin enhances the neurally induced nitrergic relaxant responses acting at the neural level.

摘要

据报道,肽类激素松弛素可通过上调神经水平的一氧化氮(NO)生物合成来降低小鼠胃底收缩反应的幅度。在本研究中,我们调查了松弛素是否也影响小鼠非肾上腺素能、非胆碱能(NANC)胃舒张反应。对处于动情前期或动情期的雌性小鼠皮下注射松弛素(1微克)或赋形剂(对照组),处理18小时。通过力位移传感器记录胃底条带的机械反应。在来自对照小鼠的卡巴胆碱预收缩条带中,在胍乙啶存在的情况下,电场刺激(EFS)引发快速舒张反应,随后可能是持续舒张。所有舒张反应均被河豚毒素消除。松弛素增加了EFS诱导的快速舒张的幅度,而不影响持续舒张或对罂粟碱的直接平滑肌反应。在NO合成抑制剂L-N(G)-硝基精氨酸(L-NNA)存在的情况下,L-NNA消除了EFS诱导的快速舒张而不影响持续舒张,松弛素无效。在来自松弛素预处理小鼠的条带中,EFS诱导的快速舒张幅度相对于对照组增强,而持续舒张以及对罂粟碱的直接平滑肌反应未改变。向浴液中进一步添加松弛素不影响神经诱导的快速舒张反应,而L-NNA则有影响。总之,在小鼠胃底,松弛素在神经水平起作用,增强神经诱导的一氧化氮能舒张反应。

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