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盐摄入量、血压与心血管结构。

Salt intake, blood pressure, and cardiovascular structure.

作者信息

Beil A H, Schmieder R E, Messerli F H

机构信息

Department of Internal Medicine-Nephrology, University of Erlangen-Nürnberg, Germany.

出版信息

Cardiovasc Drugs Ther. 1994 Jun;8(3):425-32. doi: 10.1007/BF00877918.

Abstract

Epidemiologic data revealed that a low sodium intake might have a favorable influence on blood pressure throughout an individual's lifetime. Sodium restriction was reported to lead to a modest fall in blood pressure in some studies, although a few groups of hypertensive patients experienced a rise in blood pressure. Left ventricular hypertrophy has been demonstrated to be related to cardiovascular morbidity and mortality independent of other risk factors. Dietary salt intake participates in the hypertrophic process independent of other determinants. Thus, 24-hour urinary sodium excretion has been reported to correlate with left ventricular mass independent of levels of arterial pressure. Three different mechanisms may link dietary salt intake to myocardial hypertrophy: the renin-angiotensin-aldosterone system, the sympathetic nervous system, and fluid volume homeostasis. Whether salt restriction reduces cardiovascular structural damage independent of arterial pressure has not been determined.

摘要

流行病学数据显示,低钠摄入可能在个体一生中对血压产生有利影响。在一些研究中,据报道钠限制会导致血压适度下降,尽管有几组高血压患者血压出现升高。左心室肥厚已被证明与心血管发病率和死亡率相关,且独立于其他风险因素。饮食中盐的摄入量独立于其他决定因素参与了肥厚过程。因此,据报道24小时尿钠排泄与左心室质量相关,且独立于动脉压水平。饮食中盐的摄入量与心肌肥厚可能通过三种不同机制相关联:肾素-血管紧张素-醛固酮系统、交感神经系统和体液容量稳态。限制盐摄入是否能独立于动脉压降低心血管结构损伤尚未确定。

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