Vasdev Sudesh, Gill Vicki, Parai Sushil, Gadag Veeresh
Discipline of Medicine, Faculty of Medicine Memorial University of Newfoundland St. John's, Newfoundland, A1B 3V6, Canada.
Mol Cell Biochem. 2006 Jul;287(1-2):53-60. doi: 10.1007/s11010-005-9058-6. Epub 2006 May 10.
Low alcohol intake in humans lowers the risk of coronary heart disease and may lower blood pressure. In hypertension, insulin resistance with altered glucose metabolism leads to increased formation of aldehydes. We have shown that chronic low alcohol intake decreased systolic blood pressure (SBP) and tissue aldehyde conjugates in spontaneously hypertensive rats and demonstrated a strong link between elevated tissue aldehyde conjugates and hypertension in salt-induced hypertensive Wistar-Kyoto (WKY) rats. This study investigated the antihypertensive effect of chronic low alcohol consumption in high salt-treated WKY rats and its effect on tissue aldehyde conjugates, platelet cytosolic free calcium ([Ca2+]i, and renal vascular changes. Animals, aged 7 weeks, were divided into three groups of six animals each. The control group was given normal salt diet (0.7% NaCl) and regular drinking water; the high salt group was given a high salt diet (8% NaCl) and regular drinking water; the high salt + ethanol group was given a high salt diet and 0.25% ethanol in drinking water. After 10 weeks, SBP, platelet [Ca2+]i, and tissue aldehyde conjugates were significantly higher in rats in the high salt group as compared with controls. Animals on high salt diets also showed smooth muscle cell hyperplasia in the small arteries and arterioles of the kidney. Ethanol supplementation prevented the increase in SBP and platelet [Ca2+]i and aldehyde conjugates in liver and aorta. Kidney aldehyde conjugates and renal vascular changes were attenuated. These results suggest that chronic low ethanol intake prevents salt-induced hypertension and attenuates renal vascular changes in WKY rats by preventing an increase in tissue aldehyde conjugates and cytosolic [Ca2+]i.
人类低酒精摄入量可降低冠心病风险，并可能降低血压。在高血压患者中，胰岛素抵抗伴糖代谢改变会导致醛类物质生成增加。我们已经表明，长期低酒精摄入量可降低自发性高血压大鼠的收缩压（SBP）和组织醛结合物，并证明在盐诱导的高血压Wistar-Kyoto（WKY）大鼠中，组织醛结合物升高与高血压之间存在密切联系。本研究调查了长期低酒精摄入对高盐处理的WKY大鼠的降压作用及其对组织醛结合物、血小板胞浆游离钙（[Ca2+]i）和肾血管变化的影响。将7周龄的动物分为三组，每组6只。对照组给予正常盐饮食（0.7% NaCl）和常规饮用水；高盐组给予高盐饮食（8% NaCl）和常规饮用水；高盐+乙醇组给予高盐饮食并在饮用水中添加0.25%乙醇。10周后，与对照组相比，高盐组大鼠的SBP、血小板[Ca2+]i和组织醛结合物显著升高。高盐饮食的动物在肾脏小动脉和微动脉中也出现了平滑肌细胞增生。补充乙醇可防止SBP、血小板[Ca2+]i以及肝脏和主动脉中醛结合物的增加。肾脏醛结合物和肾血管变化有所减轻。这些结果表明，长期低乙醇摄入可通过防止组织醛结合物和胞浆[Ca2+]i增加，预防盐诱导的高血压，并减轻WKY大鼠的肾血管变化。
