CARDIOVASCULAR RESPONSE TO CHRONIC ETHANOL EXPOSURE

几项使用SHR的研究未能证明 酒精在其他研究中，长期饮酒导致 减少SHR或易卒中SHR的高血压发展。 虽然研究表明，酒精管理引起轻度减少， 在血压中，作用机制仍然不清楚。 人体研究的间接证据表明， 急性和慢性酒精消费可能是由于改变 细胞内钙积累。 初步研究表明，长期饮酒的WKY和SH 大鼠抑制血压、心率和增加的组胺水平 这可能涉及细胞内钙的转移或增加的 钙离子通过电压调节进入心血管 激活钙通道。然而，长期酗酒 高血压病大鼠心肌细胞内Ca ~（2+）的变化 个人并不清楚。我们假设耐受性 心血管对长期酒精暴露的不敏感性 由钙转运到血管平滑肌的变化介导。到 为了检验这一假设，提出了以下研究： 1.慢性和急性乙醇暴露对自发性高血压大鼠钙瞬变的影响 和WKY动脉（主动脉环）平滑肌进行研究。 （假设：慢性乙醇暴露影响细胞内 SH大鼠血管平滑肌中的Ca 2+积聚）。 2.来自动脉平滑肌的Ca 2+内流的数据将与 乙醇对心率、平均动脉血 慢性和急性暴露SHR和WKY的血压和组胺水平 大鼠（假设：慢性乙醇暴露改变了Ca 2+转运 血管平滑肌中影响血压、心率 和组胺水平。 3.自发性高血压大鼠血管平滑肌（主动脉）反应性的变化 将研究慢性和急性乙醇暴露的WKY大鼠。 （假设：慢性酒精（乙醇）暴露增加Ca 2+流出 影响SH大鼠血管平滑肌的松弛）。

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).