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缓激肽对灌注大鼠肠系膜中感觉神经活动的调节作用是由一氧化氮介导的。

The regulatory effect of bradykinin on the actions of sensory nerves in the perfused rat mesentery is mediated by nitric oxide.

作者信息

Yu X J, Li Y J, Deng H W

机构信息

Department of Pharmacology, Human Medical University, People's Republic of China.

出版信息

Eur J Pharmacol. 1993 Sep 7;241(1):35-40. doi: 10.1016/0014-2999(93)90929-c.

DOI:10.1016/0014-2999(93)90929-c
PMID:8223922
Abstract

In the perfused rat mesentery, when adrenergic nerves were blocked with guanethidine and vascular smooth muscle tone was increased with methoxamine, transmural field stimulation caused a dilator response. Bradykinin significantly suppressed vasodilator responses to a transmural field stimulation in a concentration-dependent manner. After pretreatment with saponin to damage endothelial cells, bradykinin still suppressed vasodilator responses to transmural field stimulation. The effect of bradykinin was unaltered by indomethacin. N omega-Nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis, abolished the inhibition of vasodilator responses to transmural field stimulation elicited by bradykinin. However, in the presence of L-arginine and L-NAME the inhibitory effect of bradykinin reappeared. Furthermore, methylene blue itself caused potentiation of vasodilator responses to transmural field stimulation and reversed the effect of bradykinin. These findings suggest that bradykinin can produce an inhibitory modulation of the actions of sensory nerves in the perfused rat mesentery and that the effect of bradykinin may be mediated by nitric oxide released from non-adrenergic, non-cholinergic nerves.

摘要

在灌注的大鼠肠系膜中,当用胍乙啶阻断肾上腺素能神经并用甲氧明增加血管平滑肌张力时,经壁场刺激会引起舒张反应。缓激肽以浓度依赖性方式显著抑制经壁场刺激引起的血管舒张反应。在用皂素预处理损伤内皮细胞后,缓激肽仍能抑制经壁场刺激引起的血管舒张反应。缓激肽的作用不受吲哚美辛的影响。一氧化氮合成抑制剂Nω-硝基-L-精氨酸甲酯(L-NAME)消除了缓激肽对经壁场刺激引起的血管舒张反应的抑制作用。然而,在L-精氨酸和L-NAME存在的情况下,缓激肽的抑制作用再次出现。此外,亚甲蓝本身会增强经壁场刺激引起的血管舒张反应,并逆转缓激肽的作用。这些发现表明,缓激肽可对灌注大鼠肠系膜中感觉神经的作用产生抑制性调节,且缓激肽的作用可能由非肾上腺素能、非胆碱能神经释放的一氧化氮介导。

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