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α2肾上腺素能受体介导的对去脑豚鼠神经刺激诱发的神经肽Y(NPY)样免疫反应性释放的抑制作用。

Alpha 2-adrenoceptor-mediated inhibition of nerve stimulation-evoked release of neuropeptide Y (NPY)-like immunoreactivity in the pithed guinea-pig.

作者信息

Dahlöf C, Dahlöf P, Lundberg J M

出版信息

Eur J Pharmacol. 1986 Nov 19;131(2-3):279-83. doi: 10.1016/0014-2999(86)90583-2.

Abstract

Clonidine (10 micrograms X kg-1) reduced by almost 50% the increase in plasma neuropeptide (NPY)-like immunoreactivity (-LI) induced by preganglionic nerve stimulation at 8 Hz. This effect was reversed by yohimbine (1 mg X kg-1) which caused a three-fold increase of the plasma NPY-LI. Prazosin (1 mg X kg-1) had no such effect. Guanethidine (5 mg X kg-1) reduced the stimulation-evoked increase in plasma NPY-LI. It is concluded that the release of NPY-LI evoked by nerve stimulation from sympathetic nerve terminals is controlled by a presynaptic alpha 2-adrenoceptor-mediated mechanism.

摘要

可乐定(10微克/千克)使8赫兹节前神经刺激所诱导的血浆神经肽Y(NPY)样免疫反应性(-LI)增加几乎降低了50%。育亨宾(1毫克/千克)可逆转此效应,它使血浆NPY-LI增加了三倍。哌唑嗪(1毫克/千克)无此效应。胍乙啶(5毫克/千克)降低了刺激诱发的血浆NPY-LI增加。结论是,交感神经末梢神经刺激诱发的NPY-LI释放受突触前α2-肾上腺素能受体介导机制的控制。

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