CARDIOVASCULAR RESPONSE TO CHRONIC ETHANOL EXPOSURE

几项使用SHR的研究未能证明SHR的升压效应 酒精。在其他研究中，长期饮酒会导致 缓解自发性高血压或易中风的自发性高血压的发展。 尽管研究表明，饮酒会导致轻微的减少 在血压方面，其作用机制尚不清楚。 来自人体研究的间接证据表明， 急性和慢性饮酒可能是由于 细胞内钙积聚。 初步研究表明，WKY和SH的慢性饮酒 大鼠抑制血压、心率和升高的组胺水平 这可能涉及细胞内钙的转移或增加的进入 钙离子通过电压调节进入心血管血管- 激活钙通道。然而，慢性酒精的牵连 消耗对高血压患者细胞内钙离子变化的影响 对个人的理解还不是很清楚。我们假设容忍度 心血管血管对长期酒精暴露的脱敏 由钙离子转运到血管平滑肌的变化所介导。至 检验这一假设提出了以下研究： 1.慢性和急性酒精暴露对自发性高血压大鼠钙离子瞬变的影响 并对WKY动脉(主动脉环)的平滑肌进行研究。 (假设：慢性酒精暴露会影响细胞内 钙离子在SH大鼠血管平滑肌中的积聚)。 2.动脉平滑肌钙离子内流的数据将与 来自酒精对心率、平均动脉血影响的数据 慢性和急性暴露的SHR和WKY的压力和组胺水平 老鼠。(假设：慢性酒精暴露改变了钙离子的转运 血管平滑肌影响血压、心率、 以及组胺水平。 3.自发性高血压大鼠血管平滑肌(主动脉)反应性变化 将研究WKY大鼠对慢性和急性酒精暴露的影响。 (假设：长期接触酒精会增加钙离子外流 影响SH大鼠血管平滑肌的松弛作用)。

Several studies using SHRs failed to demonstrate the pressor effect of alcohol. In other studies chronic alcohol administration resulted in the attenuation of the development of hypertension in SHR or stroke-prone SHR. Although it was shown that alcohol administration caused a mild reduction in blood pressure still the mechanism of action is not understood. Indirect evidence from human studies had shown that the pressor effect of acute and chronic alcohol consumption may be due to the alteration of intracellular calcium accumulation. Preliminary studies suggest that chronic alcohol consumption in WKY and SH rats suppresses blood pressure, heart rate, and increased histamine levels which may involve a shift in intracellular calcium or increased entry of calcium into cardiovascular vessels through the regulation of voltage- activated calcium channels. However, the involvement of chronic alcohol consumption on the alteration of intracellular Ca2+ in hypertensive individuals is not clearly understood. We hypothesize that the tolerance and desensitivity of cardiovascular vessels to chronic alcohol exposure is mediated by changes in calcium transport into vascular smooth muscle. To test this hypothesis the following studies were proposed: 1. Effects of chronic and acute ethanol exposure on Ca2+ transients in SHR and WKY arterial (aorta rings) smooth muscle will be investigated. (Hypothesis: Chronic ethanol exposure affects the intracellular accumulation of Ca2+ in vascular smooth muscle of SH rats). 2. Data from Ca2+ influx of arterial smooth muscle will be correlated with data from the effects of ethanol on heart rate, mean arterial blood pressure, and histamine levels of chronic and acute exposed SHR and WKY rats. (Hypothesis: Chronic ethanol exposure alters the Ca2+ transport mechanism in vascular smooth muscle affecting blood pressure, heart rate, and histamine levels. 3. Changes in responsiveness of vascular smooth muscle (aorta) of SHR and WKY rats to chronic and acute ethanol exposure will be studied. (Hypothesis: Chronic alcohol (ethanol) exposure augments Ca2+ efflux affecting the relaxation of vascular smooth muscle in SH rats).