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犬交感神经刺激后迷走神经作用的减弱受节前α2-肾上腺素能受体调节。

Attenuation of vagal action following sympathetic stimulation is modulated by prejunctional alpha 2-adrenoceptors in the dog.

作者信息

Hall G T, Potter E K

机构信息

School of Physiology and Pharmacology, University of New South Wales, Kensington, Sydney, Australia.

出版信息

J Auton Nerv Syst. 1990 Jun;30(2):129-37. doi: 10.1016/0165-1838(90)90136-7.

Abstract

We examined the effect of the alpha 2-adrenoceptor agonist clonidine and the alpha-adrenoceptor antagonist phentolamine on the attenuation of cardiac vagal action seen following stimulation of the cardiac sympathetic nerve. In the presence of phentolamine both the maximum percentage of inhibition of cardiac vagal action and the half-time to recovery were significantly increased. In the presence of clonidine both the maximum percentage of inhibition of vagal action and the half-time to recovery were significantly reduced. The results demonstrate that the inhibition of cardiac vagal action seen following sympathetic stimulation--an effect which is attributed to actions of the co-transmitter neuropeptide Y released during sympathetic stimulation--can be modulated by drugs acting on alpha-adrenoceptors.

摘要

我们研究了α2-肾上腺素能受体激动剂可乐定和α-肾上腺素能受体拮抗剂酚妥拉明对刺激心脏交感神经后出现的心脏迷走神经作用减弱的影响。在酚妥拉明存在的情况下,心脏迷走神经作用的最大抑制百分比和恢复的半衰期均显著增加。在可乐定存在的情况下,迷走神经作用的最大抑制百分比和恢复的半衰期均显著降低。结果表明,交感神经刺激后出现的心脏迷走神经作用抑制——这种作用归因于交感神经刺激期间释放的共同递质神经肽Y的作用——可被作用于α-肾上腺素能受体的药物调节。

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