Arterial vasodilators, cardiac volume load, and cardiac hypertrophy in normotensive rats

Abstract

To assess a possible involvement of cardiac volume overload in the development of cardiac hypertrophy during chronic arterial vasodilator treatment, changes in indexes of cardiac volume load in relation to changes in cardiac anatomy were evaluated during treatment of normotensive rats with 120 mg/l hydralazine or 120 mg/l minoxidil, with drinking water. Long-term treatment with hydralazine, but not minoxidil, caused small decreases in systolic blood pressure; neither vasodilator affected heart rate with chronic treatment. Arterial vasodilator treatment for 2 wk or more resulted in increases in plasma and blood volumes by 10-20%. Both arterial vasodilators increased right atrial pressure and left ventricular end-diastolic pressure in the initial weeks of treatment. Only the minoxidil group showed a persistent increase in right atrial pressure throughout the treatment period. These hemodynamic changes were associated with increases in left ventricular (LV) internal diameter and right ventricular (RV) weight, and with minoxidil these changes were also associated with increased LV weight. LV wall thickness did not increase. Cardiac volume overload therefore indeed occurs during treatment with arterial vasodilators and may contribute to their effects on cardiac anatomy (i.e., development of RV hypertrophy and, in the case of minoxidil, also, eccentric LV hypertrophy), which are consistent with cardiac volume overload.