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高钠摄入对易卒中型自发性高血压大鼠心血管醛固酮合成的影响。

Effects of high sodium intake on cardiovascular aldosterone synthesis in stroke-prone spontaneously hypertensive rats.

作者信息

Takeda Y, Yoneda T, Demura M, Furukawa K, Miyamori I, Mabuchi H

机构信息

Second Department of Internal Medicine, School of Medicine, Kanazawa University, Japan.

出版信息

J Hypertens. 2001 Mar;19(3 Pt 2):635-9. doi: 10.1097/00004872-200103001-00017.

DOI:10.1097/00004872-200103001-00017
PMID:11327640
Abstract

OBJECTIVES

Aldosterone is synthesized in extra-adrenal tissues such as the vasculature, heart and brain. The mechanisms underlying the effect of high salt intake on the development and acceleration of vascular injury and cardiac hypertrophy in the stroke-prone spontaneously hypertensive rats (SHRSP) are still not clear. The goal of this study was to determine whether high salt intake increases cardiovascular aldosterone synthesis in SHRSP.

METHODS

Four-week-old SHRSP were given tap water or 0.9% NaCl solution for hydration for 4 weeks in addition to a normal salt diet. Isolated rat mesenteric arteries and hearts were perfused for 2 h, and the perfusate was analysed by high-performance liquid chromatography. The concentrations of aldosterone synthase gene (CYP11B2) mRNA and angiotensin II receptor (AT1R) mRNA were determined by competitive polymerase chain reaction.

RESULTS

Salt-loaded SHRSP had higher blood pressures than SHRSP with normal salt intake. Plasma aldosterone concentrations and plasma renin activity were decreased by high salt intake. Aldosterone production, the expression of CYP11B2 mRNA and AT1R mRNA in mesenteric arteries and hearts were significantly increased by high salt intake.

CONCLUSIONS

These results suggest that high salt intake increases aldosterone production and expression of the AT1R mRNA in the cardiovascular tissue in SHRSP, which may contribute to the development of malignant hypertension in salt-loaded SHRSP.

摘要

目的

醛固酮在诸如血管、心脏和大脑等肾上腺外组织中合成。高盐摄入对易卒中自发性高血压大鼠(SHRSP)血管损伤发展和加速以及心脏肥大的影响机制仍不清楚。本研究的目的是确定高盐摄入是否会增加SHRSP心血管组织中醛固酮的合成。

方法

除正常盐饮食外,给4周龄的SHRSP饮用自来水或0.9% NaCl溶液进行水合作用4周。对分离的大鼠肠系膜动脉和心脏进行2小时灌注,并用高效液相色谱法分析灌注液。通过竞争性聚合酶链反应测定醛固酮合酶基因(CYP11B2)mRNA和血管紧张素II受体(AT1R)mRNA的浓度。

结果

高盐饮食的SHRSP血压高于正常盐摄入的SHRSP。高盐摄入可降低血浆醛固酮浓度和血浆肾素活性。高盐摄入显著增加了肠系膜动脉和心脏中醛固酮的产生、CYP11B2 mRNA和AT1R mRNA的表达。

结论

这些结果表明,高盐摄入增加了SHRSP心血管组织中醛固酮的产生和AT1R mRNA的表达,这可能有助于高盐饮食的SHRSP发生恶性高血压。

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