Sodium intake modulates the development of cardiac hypertrophy in two-kidney, one clip rats.

Abstract

Sodium homeostasis exerts a powerful influence on the cardiovascular system in normotensive and hypertensive animals. Previous studies indicate that factors other than blood pressure can influence cardiac hypertrophy. In the present experiments, we evaluated the effects of different sodium diets in the two-kidney, one clip hypertension model in the rat. After the renal artery had been cupped, the rats received a normal sodium (177 meq/kg), high sodium (517 meq/kg), and low sodium (7 meq/kg) diet during 4 weeks. The final blood pressure was almost the same in the three groups (normal sodium 170 ±12 mm Hg; low sodium 168 ±4 mm Hg; and high sodium 162 ±7 mm Hg). Sodium restriction significantly reduced the development of cardiac hypertrophy as compared with rats on normal or high sodium diets. Thus, ventricular weight and ventricular weight/body weight ratio were significantly higher in rats subjected to a normal or high sodium diet (p<0.01). The hypertrophied hearts of rats on normal and high sodium diets showed a larger increase in the number of cardiac ^-adrenergk receptors than those observed in hearts from low sodium diet, clipped rats. These results show that sodium modulates the development of cardiac hypertrophy in two-kidney, one clip hypertensive rats. Similarly, the cardiac /3-adrenergic receptors appear to be influenced by dietary sodium intake. A possible role of the sympathetic nervous system is suggested. (Hypertension 1990;15(suppl I):I-157-I-160)

Excessive dietary salt promotes aortic stiffness in murine renovascular hypertension

“…Experimentally, dietary salt loading has been repeatedly demonstrated to increase and exaggerate ABP in multiple experimental models including Dahl salt-sensitive rats ( 22 , 38 ), deoxycorticosterone acetate-salt ( 23 , 25 ), chronic infusion of angiotensin II ( 28 ), and reduced renal mass ( 18 , 19 , 21 ). In regard to 2K1C models of renovascular hypertension, the majority of studies report that a high-NaCl diet does not exaggerate ABP ( 10 , 15 , 35 , 49 , 51 ). However, these previous studies largely relied on tail-cuff measurements of ABP or ABP measurements at a single time point.…”

“…Furthermore, the time of dietary salt manipulation may represent another important factor. Previous studies ( 10 , 15 , 35 , 49 , 51 ) administered salt diets either at the time of renal artery clipping or after the establishment of hypertension rather than acclimating animals to the respective diet to mimic chronic dietary salt consumption in clinical populations.…”

Hydrogen Sulfide Inhibits High-Salt Diet-Induced Myocardial Oxidative Stress and Myocardial Hypertrophy in Dahl Rats

“…The study showed that salt-sensitive hypertensive patients were more prone to develop myocardial hypertrophy and cardiovascular events (Chamarthi et al, 2010). Previous studies suggested that the potential mechanisms underlying high-salt-induced myocardial hypertrophy mainly included hemodynamic changes, sodium serum levels, increased sodium influx of cardiomyocytes, activation of cardiac renin-angiotensin-aldosterone system (RAAS) and activation of cardiac sympathetic nervous system (Gallo et al, 1990; Galderisi et al, 1991; Harmsen and Leenen, 1992; Le Corvoisier et al, 2010; He and Macgregor, 2012). However, the mechanism for high-salt-induced myocardial hypertrophy still remains unclear.…”

Effect of Dietary Sodium Chloride on the Development of Renal Glomerular and Vascular Lesions in Hypertensive Rats

“…A dissociation between blood pressure and cardiac hypertrophy in 2K1C rats has been reported (Lindpaintner & Sen 1985;Gallo et al 1990). In their studies, sodium restriction resulted in reversal of cardiac hypertrophy but did not lower blood pressure.…”