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酒精对血压以及血管醛固酮和皮质酮生成的影响。

Effects of alcohol on blood pressure and production of vascular aldosterone and corticosterone.

作者信息

Zhang Y, Sun T, Jiang F, Chu L, Yu W, Wei L, Pang J, Liu Y, Su G

机构信息

Department of Cardiology, 401th Hospital, Qingdao, People's Republic of China.

出版信息

Horm Res. 2001;55(5):245-8. doi: 10.1159/000050004.

Abstract

AIMS

The aims of this study were to search for the role of alcohol in blood pressure regulation in rats and to investigate the effects of alcohol on the production of vascular aldosterone and corticosterone.

METHODS

Male Wistar rats received alcohol 0.7 g x kg(-1) x day(-1) (alcohol-treated group 1) or 1.4 g x kg(-1) x day(-1) (alcohol-treated group 2) or 2.1 g x kg(-1) x day(-1) (alcohol-treated group 3), orally, for 3 months, and blood pressure was monitored by a pressure transducer. Systolic blood pressure increased in Wistar rats treated with alcohol compared to control rats. Mesenteric artery perfusion ex vivo was performed and pressor responses to norepinephrine were determined. The pressor responses to norepinephrine in mesenteric arteries treated with alcohol were significantly increased. The perfusate from the mesenteric arteries was collected and applied to a Sep-Pak C 18 cartridge column for reverse-phase high-performance liquid chromatography and aldosterone and corticosterone levels were determined by radioimmunoassay, aldosterone was decreased but corticosterone was increased in the perfusate from arteries treated with alcohol.

RESULTS

Reverse transcriptase polymerase chain reaction showed that alcohol inhibited the expression of 11beta-HSD2 and CYP11B2 mRNA in mesenteric arteries.

CONCLUSIONS

These results reveal that alcohol is able to induce hypertension and provide evidence that alcohol inhibits the transcriptions of both 11beta-HSD2 and CYP11B2 in the vasculature, leading to lower aldosterone and higher corticosterone production in vessels, and increased vasoconstrictor responses to norepinephrine.

摘要

目的

本研究旨在探寻酒精在大鼠血压调节中的作用,并研究酒精对血管醛固酮和皮质酮生成的影响。

方法

雄性Wistar大鼠口服0.7 g·kg⁻¹·d⁻¹酒精(酒精处理组1)或1.4 g·kg⁻¹·d⁻¹酒精(酒精处理组2)或2.1 g·kg⁻¹·d⁻¹酒精(酒精处理组3),持续3个月,通过压力传感器监测血压。与对照大鼠相比,酒精处理的Wistar大鼠收缩压升高。进行离体肠系膜动脉灌注并测定对去甲肾上腺素的升压反应。酒精处理的肠系膜动脉对去甲肾上腺素的升压反应显著增强。收集肠系膜动脉的灌注液,应用于Sep-Pak C 18柱进行反相高效液相色谱分析,通过放射免疫测定法测定醛固酮和皮质酮水平,酒精处理的动脉灌注液中醛固酮降低但皮质酮升高。

结果

逆转录聚合酶链反应显示酒精抑制肠系膜动脉中11β-HSD2和CYP11B2 mRNA的表达。

结论

这些结果表明酒精能够诱发高血压,并提供证据表明酒精抑制血管中11β-HSD2和CYP11B2的转录,导致血管中醛固酮生成降低和皮质酮生成增加,以及对去甲肾上腺素的血管收缩反应增强。

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