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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Activation of the central histaminergic system mediates arachidonic-acid-induced cardiovascular effects
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Activation of the central histaminergic system mediates arachidonic-acid-induced cardiovascular effects

机译：中枢组胺能系统的激活介导花生四烯酸诱导的心血管作用

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摘要

The aim of this study was to explain the involvement of the central histaminergic system in arachidonic acid (AA)-induced cardiovascular effects in normotensive rats using hemodynamic, immunohistochemistry, and microdialysis studies. Intracerebroventricularly (i.c.v.) administered AA (0.25, 0.5, and 1.0 μmol) induced dose- and time-dependent increases in mean arterial pressure and decreased heart rate in conscious normotensive Sprague-Dawley rats. Central injection of AA (0.5 μmol) also increased posterior hypothalamic extracellular histamine levels and produced strong COX-1 but not COX-2 immunoreactivity in the posterior hypothalamus of rats. Moreover, the cardiovascular effects and COX-1 immunoreactivity in the posterior hypothalamus induced by AA (0.5 μmol; i.c.v.) were almost completely blocked by the H2 receptor antagonist ranitidine (50 and 100 nmol; i.c.v.) and partially blocked by the H1 receptor blocker chlorpheniramine (100 nmol; i.c.v.) and the H3-H4 receptor antagonist thioperamide (50 and 100 nmol; i.c.v.). In conclusion, these results indicate that centrally administered AA induces pressor and bradycardic responses in conscious rats. Moreover, we suggest that AA may activate histaminergic neurons and increase extracellular histamine levels, particularly in the posterior hypothalamus. Acting as a neurotransmitter, histamine is potentially involved in AA-induced cardiovascular effects under normotensive conditions.
机译：这项研究的目的是通过血液动力学，免疫组织化学和微透析研究来解释中枢组胺能系统在降血压大鼠中花生四烯酸（AA）引起的心血管效应中的作用。在有意识的血压正常的Sprague-Dawley大鼠中，脑室内（i.c.v.）施用AA（0.25、0.5和1.0μmol）导致平均动脉压剂量依赖性和时间依赖性增加，心率降低。中央注射AA（0.5μmol）也会增加大鼠下丘脑后下丘脑细胞外组胺的水平，并产生强的COX-1免疫反应性，但不产生COX-2免疫反应性。此外，由AA（0.5μmol; icv）诱导的下丘脑后部的心血管效应和COX-1免疫反应性几乎完全被H2受体拮抗剂雷尼替丁（50和100 nmol; icv）阻断，而部分被H1受体阻断剂氯苯那敏阻断（100 nmol; icv）和H3-H4受体拮抗剂硫代过酰胺（50和100 nmol; icv）。总之，这些结果表明，在有意识的大鼠中，集中施用AA会诱导升压和心动过缓反应。此外，我们建议AA可能激活组胺能神经元并增加细胞外组胺水平，尤其是在下丘脑后部。组胺作为一种神经递质，可能在血压正常的情况下参与AA诱导的心血管作用。

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