Why the study?
Does dietary salt content modulate cardiac function and Ca2+ handling proteins in spontaneously hypertensive rats?
Does dietary salt content modulate cardiac function and Ca2+ handling proteins in spontaneously hypertensive rats?
Long-term modulation of dietary salt intake alters cardiac Ca2+ handling proteins, which may underlie its effects on myocardial function and hypertrophy in hypertension.
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Should not alter salt recommendations in hypertension; leaves open whether dietary salt modulates cardiac Ca2+ handling proteins in humans.
BACKGROUND: High sodium intake contributes to the pathogenesis of hypertension and adversely affects cardiac function. Conversely, sodium reduction is associated with a blood pressure decrease and improved cardiovascular function. However, the mechanisms that underlie the cardiac effects induced by salt intake in hypertension have not been fully elucidated. Ca2+ handling is critical for efficient myocardial function; thus, we aimed to investigate the long-term effects of diets with different salt contents on cardiac function and Ca2+ handling proteins in spontaneously hypertensive rats (SHRs). METHODS: Cardiac function was evaluated by catheterization. Ca2+ handling and contractile proteins were evaluated by immunoblotting in hearts from SHRs fed for 6 months with diets containing high (HS, 3%), low (LS, 0.03%), or normal salt content (NS, 0.3%). Diets were introduced immediately after weaning. Tail cuff pletismography was assessed at the 3rd and 7th months of follow-up. RESULTS: Compared to the NS group, the HS group exhibited worsened hypertension, increased cardiac expression of β-myosin heavy chain (MHC), a decreased α/β-MHC ratio and reduced expression of both phospholamban (PLB) and Na+/Ca2+ exchanger (NCX). LS intake attenuated the blood pressure increase and left ventricle hypertrophy, slightly decreased the cardiac contractility and relaxation index, and increased the α/β-MHC ratio. These effects were accompanied by increased cardiac PLB expression and decreased Ca2+ L-type channel and NCX expression. CONCLUSIONS: These findings indicate that the modulation of Ca2+ handling may be one of the molecular mechanisms underlying the effect of salt intake on myocardial function in hypertension.
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Berger et al. (2018) studied this question.
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