Role of sodium in hypertensive cardiac hypertrophy

Abstract

Cardiac hypertrophy in systemic hypertension may not result simply from increased afterload. Previous studies indicate that factors other than blood pressure may influence cardiac hypertrophy. We evaluated the effects of dietary sodium restriction in two-kidney one-clip renal hypertensive rats. After the renal artery had been clipped, the rats received a normal diet until hypertension was established; thereafter, a sodium-deficient diet was instituted in one group. Clipped rats on a regular diet had significantly higher systolic blood pressures than sham-operated controls (205 ± 9 vs 129 ± 1 mm Hg, respectively). Sodium restriction did not reverse hypertension (190 ± 8 mm Hg), but led to a significant reduction of relative heart weight compared to rats on the normal diet (2.94 ± 0.24 vs 3.86 ± 0.23 mg/g, respectively; P < 0.01). The hypertrophied hearts of animals on the regular diet showed depressed tissue catecholamines (significant only for norepinephrine); sodium restriction resulted in a restoration to normal levels. Thus, we demonstrated a dissociation of blood pressure and cardiac hypertrophy in the two-kidney one-clip model, similar to previous findings in other models. Our results support the concept that factors other than blood pressure contribute to cardiac hypertrophy. Dietary sodium intake appears to be one such factor. In addition, a possible role of the sympathetic nervous system is suggested.