Abstract 11352: Dietary Sodium Restriction Results in Early Neurohormonal Activation in Experimental Progressive Heart Failure
Background: Dietary sodium restriction has traditionally been a mainstay in the management of heart failure (HF), but the modulating action of dietary sodium excess or restriction on neurohormonal adaptations during the progression of HF is poorly defined. The objective of this investigation was to assess the role of dietary sodium in early HF utilizing a novel large animal model of compensated HF.
Methods: Experimental systolic HF was produced in a canine model by rapid right ventricular pacing. Dogs were fed one of the three diets: 1) high sodium diet [250 mEq (5.8 grams) per day, n=6]; 2) a normal sodium diet [58 mEq (1.3 grams) per day, n=6]; and 3) a sodium restricted diet [11 mEq (0.25 grams) per day, n=6]. During the period of this study hemodynamic and neuro-endocrine parameters were measured.
Results: Decreases in CO and MAP and increases in RAP, PAP, PCWP, SVR and PVR were similar in all three sodium diet groups. Progressive neurohormonal activation was demonstrated in all three groups, however, dietary sodium restriction, in contrast to normal and high sodium groups, resulted in early (10 days HF) activation of circulating vasoconstrictors including plasma renin (5.2 ± 1.0 vs. 1.8 ± 1.0 vs. 2.3 ± 1.7 ng/ml/hr, p<0.05), aldosterone (18 ± 5 vs. 3.8 ± 0.8 vs. 2.7 ± 0.2 ng/dl, p<0.05), norepinephrine (317 ± 53 vs. 206 ± 12 vs. 204 ± 47 pg/ml, p<0.05) and epinephrine (324 ± 76 vs. 134 ± 24 vs. 96 ± 22 pg/ml, p<0.05). Also, as compared to the high sodium diet, sodium restriction resulted at HF day 17 in activation of ANP (535 ± 101 vs. 196 ± 57 pg/ml, p<0.05). In marked contrast, the high sodium diet demonstrated significant suppression of neuroendocrine activation over the entire course of HF progression including marked suppression of both the RAA and adrenergic nervous systems.
Conclusions: Excessive dietary sodium restriction in early stage HF results in early neuroendocrine activation and decompensation, while a normal , as well as, high dietary sodium are associated with delayed neurohormonal activation during the progression of HF. These studies warrant further evaluation in humans to determine if dietary sodium restriction particularly during early stage B HF may have a detrimental effect on disease progression secondary to neurohormonal mechanisms.
- © 2012 by American Heart Association, Inc.