Luo X X, Wen A D, Guo Z A, Tan Y H
Department of Pharmacology, Xijing Hospital, Fourth Military Medical University, Xi-an, China.
Zhongguo Yao Li Xue Bao. 1996 Sep;17(5):425-8.
To study the histamine H3 receptors mediated inhibition of norepinephrine (NE) release from cardiac sympathetic terminals of guinea pig isolated atria.
Release of NE induced by electric field stimulation (50 mA, 5 ms) in the bath solution was measured by HPLC-ECD.
The release of NE caused by field stimulation was attenuated by (R)-alpha-methyl-histamine (alpha-MeHA, 0.1 nmol.L-1(-10) mumol.L-1) in a concentration-dependent manner. Thioperamide concentration-dependently antagonized the inhibition of alpha-MeHA. Blockade of H1, H2, alpha 2, beta 2-receptors failed to prevent the inhibitory effect of alpha-MeHA. Thioperamide (1 nmol.L-1(-10) mumol.L-1), when used alone, concentration-dependently facilitated the release of NE evoked by field stimulation.
The presynaptic histamine H3-receptors inhibited the NE release from cardiac sympathetic terminals.
研究组胺H3受体介导的对豚鼠离体心房心脏交感神经末梢去甲肾上腺素（NE）释放的抑制作用。
通过高效液相色谱-电化学检测法（HPLC-ECD）测量浴液中电场刺激（50 mA，5 ms）诱导的NE释放。
（R）-α-甲基组胺（α-MeHA，0.1 nmol·L-1至10 μmol·L-1）以浓度依赖性方式减弱电场刺激引起的NE释放。硫丙拉嗪浓度依赖性地拮抗α-MeHA的抑制作用。阻断H1、H2、α2、β2受体未能阻止α-MeHA的抑制作用。硫丙拉嗪（1 nmol·L-1至10 μmol·L-1）单独使用时，浓度依赖性地促进电场刺激诱发的NE释放。
突触前组胺H3受体抑制心脏交感神经末梢的NE释放。
