DIETARY-SODIUM INTAKE AND LEFT-VENTRICULAR HYPERTROPHY IN NORMOTENSIVE RATS

In three different normotensive rat strains, we evaluated the effects of a large range of dietary sodium (101, 342, and 1,370-mu-mol Na+/g) on cardiac structure in relation to age of the rats and to changes in central hemodynamics and cardiac sympathetic neuronal activity. In young, 4-wk-old Wistar-Kyoto rats (WKY) an increase in dietary sodium induced a dose-related increase in left ventricular (LV) weight (+10 and +24% after 4 wk of 342 or 1,370-mu-mol Na+/g diets, respectively). Young Wistar rats also developed LV hypertrophy (+14%) on a high sodium intake, but this was less than that seen in WKY. In more mature Wistar and WKY rats, the extent of this trophic response to high sodium intake diminished. In contrast to young Wistar and WKY rats, Dahl salt-resistant rats did not show a trophic response with initiation of high sodium intake at 4 wk of age. The cardiac trophic response to dietary sodium was not associated with changes in central hemodynamics (i.e., filling pressures, cardiac output, and blood pressure). Norepinephrine turnover rate of the left ventricle tended to decrease in response to high dietary sodium intake. We conclude that food sodium can significantly increase LV weight depending on the strain and age of the rats and that this trophic response occurs independent of cardiac volume or pressure overload.