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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Central benzodiazepine involvement in clonidine cardiovascular actions.
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Central benzodiazepine involvement in clonidine cardiovascular actions.

机译：中枢苯二氮卓参与可乐定的心血管作用。

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It is well known that the GABAergic and noradrenergic systems play an important role in blood pressure and heart rate regulation. Benzodiazepines and beta-carbolines, respectively, increase or decrease the probability of chloride-channel opening induced by GABA. The aim of this study was to determine, in conscious rats, the interaction existing between the central alpha2-adrenoceptor stimulation induced by clonidine and the facilitation or impairment of benzodiazepine receptor activity through the administration of either diazepam, a benzodiazepine receptor agonist, or methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM), an inverse benzodiazepine agonist. Clonidine (5-10 microg, intracerebroventricularly) reduced heart rate and increased mean blood pressure by activation of central alpha2-adrenoceptors. Diazepam (2 mg/kg, intravenously (i.v.)) induced an increase in heart rate, while DMCM (0.3 mg/kg, i.v.) elicited a bradycardic effect. The bradycardic effects induced by both clonidine and DMCM were antagonized by the prior administration of methylatropine (1.5 mg/kg, i.v.). DMCM (0.3 mg/kg, i.v.) prevented the clonidine effects on heart rate and mean blood pressure, while diazepam (2 mg/kg, i.v.) failed to modify these effects. Our results suggest that the bradycardic effects of clonidine are mediated by a vagal stimulation and are related to the activation of a GABAergic pathway.
机译：众所周知，GABA能和去甲肾上腺素能系统在血压和心率调节中起重要作用。苯二氮卓类和β-咔啉类分别增加或减少GABA诱导氯离子通道打开的可能性。这项研究的目的是确定在有意识的大鼠中，可乐定诱导的中央α2-肾上腺素能受体刺激与通过给予地西epa，苯并二氮杂pine受体激动剂或甲基6促进或损害苯二氮杂pine受体活性之间存在的相互作用。 ，7-二甲氧基-4-乙基-β-咔啉-3-羧酸酯（DMCM），苯二氮卓类反向激动剂。可乐定（5-10微克，脑室内）可通过激活中央α2-肾上腺素受体降低心率并增加平均血压。地西p（2 mg / kg，静脉内（i.v.））引起心率增加，而DMCM（0.3 mg / kg，i.v.）引起心动过缓。在先服用甲基阿托品（1.5 mg / kg，静脉注射）可乐定可乐定和DMCM诱导的心动过缓。 DMCM（0.3 mg / kg，静脉内）预防了可乐定对心率和平均血压的影响，而地西epa（2 mg / kg，静脉内）未能改变这些作用。我们的结果表明，可乐定的心动过缓作用由迷走神经刺激介导，并且与GABA能途径的激活有关。

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