组胺H3受体抑制豚鼠心肌中的交感神经传递。
Histamine H3-receptors inhibit sympathetic neurotransmission in guinea pig myocardium.
作者信息
Luo X X, Tan Y H, Sheng B H
机构信息
Department of Pharmacology, Fourth Military Medical University, Xian, China.
出版信息
Eur J Pharmacol. 1991 Nov 12;204(3):311-4. doi: 10.1016/0014-2999(91)90857-m.
The histamine H3 agonist, (R)-alpha-methylhistamine (alpha-MeHA, 10(-10) to 10(-5) M), caused a concentration-dependent inhibition of the sympathetic contractile response to electrical field stimulation of guinea pig isolated atria, but alpha-MeHA did not alter the basal tension or the contraction induced by exogenously applied norepinephrine. Blockade of H1 and H2 histamine receptors, and alpha- and beta-adrenoceptors failed to prevent the inhibitory effect of alpha-MeHA, whereas the specific H3 receptor antagonist, thioperamide, concentration dependently reversed the inhibitory effect of alpha-MeHA. At the concentration of 10(-7) M, which was effective for antagonizing the action of alpha-MeHA, thioperamide did not modify the sympathetic responses facilitated by the beta 2-adrenoceptor agonist, clenbuterol, or attenuated by the alpha 2-adrenoceptor agonist, clonidine. Our results suggest that H3 receptors exist on the cardiac sympathetic terminals, which may modulate adrenergic neurotransmission in guinea pig myocardium.
组胺H3激动剂（R）-α-甲基组胺（α-MeHA，10⁻¹⁰至10⁻⁵M）对豚鼠离体心房电场刺激引起的交感收缩反应产生浓度依赖性抑制，但α-MeHA不改变基础张力或外源性应用去甲肾上腺素诱导的收缩。组胺H1和H2受体以及α和β肾上腺素能受体的阻断未能阻止α-MeHA的抑制作用，而特异性H3受体拮抗剂硫代哌啶浓度依赖性地逆转了α-MeHA的抑制作用。在10⁻⁷M浓度下，硫代哌啶可有效拮抗α-MeHA的作用，且不改变β2肾上腺素能受体激动剂克伦特罗促进的或α2肾上腺素能受体激动剂可乐定减弱的交感反应。我们的结果表明，心脏交感神经末梢存在H3受体，其可能调节豚鼠心肌中的肾上腺素能神经传递。
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