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The role of sodium in hypertension is more complex than simply elevating arterial pressure

Abstract

Excessive salt intake exacerbates hypertension and further increases left-ventricular mass in clinical essential and experimental hypertension. Additionally, a growing body of evidence strongly suggests that high dietary salt loading exerts detrimental cardiac effects independently of its hemodynamic load. The clinical evidence of cardiac structural and functional alterations associated with salt is, however, scarce. In order to explore the purported beliefs in humans, in this review we draw on our experimental studies in naturally occurring hypertension and discuss the clinical implications of the nonhemodynamic mechanisms underlying these salt-related changes.

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Figure 1: Systolic arterial pressure and left-ventricular geometry in salt-loaded younger (16 weeks) and older (52 weeks) adult spontaneously hypertensive rats
Figure 2: Left-ventricular hydroxyproline concentration in spontaneously hypertensive rats receiving high-salt diet
Figure 3: Echocardiografically measured systolic and diastolic function in spontaneously hypertensive rats fed with an 8% salt diet
Figure 4: Deceleration time of mitral E wave and left-ventricular filling pressure

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Correspondence to Edward D Frohlich.

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Frohlich, E., Varagic, J. The role of sodium in hypertension is more complex than simply elevating arterial pressure. Nat Rev Cardiol 1, 24–30 (2004). https://doi.org/10.1038/ncpcardio0025

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