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首页> 外文期刊>Life sciences >Chronic ethanol attenuates centrally-mediated hypotension elicited via alpha(2)-adrenergic, but not I(1)-imidazoline, receptor activation in female rats.
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Chronic ethanol attenuates centrally-mediated hypotension elicited via alpha(2)-adrenergic, but not I(1)-imidazoline, receptor activation in female rats.

机译：慢性乙醇减弱雌性大鼠中通过alpha（2）-肾上腺素而不是I（1）-咪唑啉受体激活引起的中枢介导的低血压。

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AIMS: This study dealt with the effect of chronic ethanol administration on hemodynamic responses elicited by alpha(2)-adrenergic (alpha-methyldopa) or I(1)-imidazoline (rilmenidine) receptor activation in telemetered female rats. MAIN METHODS: The effects of alpha-methyldopa or rilmenidine on blood pressure (BP), heart rate (HR) and their variability were investigated in rats that received liquid diet without or with ethanol (5% w/v) for 12 weeks. To evaluate the effect of each drug on cardiovascular autonomic control (BP and HR variability) in the absence or presence of ethanol, three time-domain indices of hemodynamic variability were measured: (i) standard deviation of mean arterial pressure (SDMAP), (ii) standard deviation of beat-to-beat intervals, and (iii) root mean square of successive differences in R-R intervals. KEY FINDINGS: In liquid diet-fed control rats, i.p. rilmenidine (600 microg/kg) or alpha-methyldopa (100 mg/kg) reduced BP along with decreases and increases, respectively, in HR. Both drugs had no effect on HR variability but reduced BP variability (SDMAP), suggesting a reduced vasomotor sympathetic tone. Ethanol feeding attenuated reductions in BP and SDMAP evoked by alpha-methyldopa but not by rilmenidine. SIGNIFICANCE: We conclude that chronic ethanol preferentially compromises alpha(2)- but not I(1)-receptor-mediated hypotension in female rats probably via modulation of vasomotor sympathetic activity. These findings highlight the adequacy of rilmenidine use to lower BP in hypertensive alcoholic females.
机译：目的：这项研究涉及遥测雌性大鼠中长期使用乙醇对由α（2）-肾上腺素能（α-甲基多巴）或I（1）-咪唑啉（rilmenidine）受体引起的血液动力学反应的影响。主要方法：在接受无糖或含乙醇（5％w / v）的流食的大鼠中，研究了α-甲基多巴或瑞美尼定对血压，心率（HR）及其变异性的影响，持续12周。为了评估在无乙醇存在下每种药物对心血管自主控制（BP和HR变异性）的影响，测量了三个时域血流动力学变异性指标：（i）平均动脉压标准差（SDMAP），（ ii）逐拍间隔的标准偏差，以及（iii）RR间隔连续差的均方根。主要发现：在以液体饮食喂养的对照大鼠中，腹腔注射瑞美尼定（600 microg / kg）或α-甲基多巴（100 mg / kg）降低BP，并分别降低和增加HR。两种药物对HR变异性均无影响，但降低了BP变异性（SDMAP），提示血管舒缩性交感神经张力降低。乙醇进食减弱了由α-甲基多巴引起的BP和SDMAP降低，但未被利美替丁引起。意义：我们得出的结论是，慢性乙醇可能通过调节血管舒缩交感神经活动而优先损害雌性大鼠的α（2）-而非I（1）-受体介导的低血压。这些发现凸显了使用来美尼定可降低高血压酒精中毒女性的血压。

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