Influence of Long-Term Salt Diets on Cardiac Ca2+ Handling and Contractility Proteins in Hypertensive Rats

Berger, Rebeca Caldeira Machado; Benetti, Acaris; Girardi, Adriana Castello Costa; Forechi, Ludimila; Oliveira, Rafaella Martins de; Vassallo, Paula Frizera; Mill, José Geraldo

doi:10.1093/ajh/hpy023

Cited by 6 publications

(6 citation statements)

References 36 publications

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“…Changes in the proportion of these protein filaments are associated with cardiac mechanical performance. A high sodium diet is associated with an increase in cardiac expression of β-MHC and a decrease in the α/β-MHC ratio [48]. A low sodium diet was seen to be associated with increased α/β-MHC ratio, which in turn improves myocardial mechanical performance [48].…”

Section: Potential Molecular Mechanism Of Salt Diet and Heart Failurementioning

confidence: 99%

“…A high sodium diet is associated with an increase in cardiac expression of β-MHC and a decrease in the α/β-MHC ratio [48]. A low sodium diet was seen to be associated with increased α/β-MHC ratio, which in turn improves myocardial mechanical performance [48]. Similar effects of a high sodium diet were seen to be associated with myocyte enhancer factor (MEF) 2/nuclear factor of activated T cell (NFAT) transcriptional activity, and thereby increasing the expression of MHC genes [49].…”

Section: Potential Molecular Mechanism Of Salt Diet and Heart Failurementioning

confidence: 99%

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Sodium Intake and Heart Failure

Patel

Joseph

2020

IJMS

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Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β—myosin heavy chain, decreased expression of α/β—myosin heavy chain, increased myocyte enhancer factor 2/nuclear factor of activated T cell transcriptional activity, and increased salt-inducible kinase 1 expression, which leads to alteration in myocardial mechanical performance. A high sodium diet is also associated with alterations in various proteins responsible for calcium homeostasis and myocardial contractility. Excessive sodium intake is associated with the development of a variety of comorbidities including hypertension, chronic kidney disease, stroke, and cardiovascular diseases. While the American College of Cardiology/American Heart Association/Heart Failure Society of America guidelines recommend limiting sodium intake to both prevent and manage heart failure, the evidence behind such recommendations is unclear. Our review article highlights evidence and underlying mechanisms favoring and contradicting limiting sodium intake in heart failure.

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Section: Potential Molecular Mechanism Of Salt Diet and Heart Failurementioning

confidence: 99%

Section: Potential Molecular Mechanism Of Salt Diet and Heart Failurementioning

confidence: 99%

Sodium Intake and Heart Failure

Patel

Joseph

2020

IJMS

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“… 19 , 20 , 21 , 23 In addition, a direct influence of dietary sodium on the myocardial function by interfering with myocyte calcium handling has been postulated. 29 Another issue potentially determining the mechanisms behind cardiac effects and degree of responses to diet may be patient body weight and blood pressure status.…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, changes in insulin sensitivity, LV afterload, and renin–angiotensin–aldosterone and sympathetic system activation, as well as antioxidant defence in the heart, should be considered as potential contributors 3,26–28 . In addition, a direct influence of dietary sodium on the myocardial function by interfering with myocyte calcium handling has been postulated 29 . Another issue potentially determining the mechanisms behind cardiac effects and degree of responses to diet may be patient body weight and blood pressure status.…”

Section: Discussionmentioning

confidence: 99%

“…7,8 Under healthy circumstances, insulin exerts robust vasodilatory actions in the skeletal muscle microvasculature, and an impairment in this physiologic response promotes IR. 22 A number of subcellular mechanisms mediating the effect of high sodium on muscle perfusion have been proposed, including impaired Na + /K + -ATPase expression regulation, reduced activity of epithelial sodium channels in endothelial cells, and abnormal caveolin-1-endothelial nitric oxide synthase interaction, all of which produce increased endothelial stiffness and blunted vascular relaxation. 23,24 The promotion of IR by high sodium diet can also be mediated by other, non-vascular derived mechanisms, including the development of leptin resistance, hyperphagia, and increase in body fat content.…”

Section: Sodium Intake Skeletal Muscle Perfusion and Insulin Resistancementioning

confidence: 99%

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Role of skeletal muscle perfusion and insulin resistance in the effect of dietary sodium on heart function in overweight

et al. 2021

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Aims Weight excess and insulin resistance predispose to heart failure. High sodium consumption may contribute to the development of cardiac impairment in insulin‐resistant individuals by promoting inadequate skeletal muscle microvascular perfusion response to insulin. We sought to investigate the association of dietary sodium reduction with muscle perfusion, insulin sensitivity, and cardiac function in overweight/obese insulin‐resistant (O‐IR) normotensive subjects. Methods and results Fifty O‐IR individuals with higher than recommended sodium intake were randomized to usual or reduced sodium diet for 8 weeks; 25 lean, healthy subjects served as controls for pre‐intervention measurements. Echocardiography and muscle perfusion were performed during fasting and under stable euglycaemic–hyperinsulinaemic clamp conditions. O‐IR patients demonstrated subclinical cardiac dysfunction as evidenced by lower left ventricular global longitudinal strain (GLS), e′ tissue velocity, and left atrial strain and reduced muscle perfusion. The intervention arm showed improvements in insulin resistance [glucose infusion rate (GIR)], GLS, e′, atrial strain, and muscle perfusion in fasting conditions, as well as improved responses of GLS and muscle perfusion to insulin during clamp. Significant interactions were found between the allocation to low‐salt diet and improvement in muscle perfusion on change in GIR at follow‐up (P = 0.030), and between improvement in muscle perfusion and change in GIR on change in GLS response to insulin at follow‐up (P = 0.026). Mediation analysis revealed that the relationship between the reduction of sodium intake and improvement in GLS was mediated by improvements in muscle perfusion and GIR (decrease in beta coefficient from −0.29 to −0.16 after the inclusion of mediator variables to the model). Conclusions The reduction of dietary sodium in the normotensive O‐IR population improves cardiac function, and this effect may be associated with the concomitant improvements in skeletal muscle perfusion and insulin resistance. These findings might contribute to refining heart failure preventive strategies.

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