Chronic arterial vasodilation, central hemodynamics, and cardiac hypertrophy in spontaneously hypertensive rats

To determine the possible contribution of cardiac volume overload in the failure of arterial vasodilators to induce regression of left ventricular hypertrophy (LVH), we evaluated in spontaneously hypertensive rats (SHRs) the changes in central hemodynamics caused by treatment with hydralazine or minoxidil. Cardiac output measured by the thermodilution technique and filling pressures were measured in conscious, freely moving rats. Increases in cardiac output were observed after 1 day of treatment, and persisted during chronic treatment; ganglionic blockade did not affect this increase. However, the LV end-diastolic pressure and right atrial pressure of SHRs were not increased by hydralazine or minoxidil. Minoxidil increased the LV weight, and decreased the LV wall thickness to LV internal radius ratio, whereas hydralazine did not change these parameters. We conclude that in SHRs changes in filling pressures do not represent the primary stimulus for the persistence or progression of cardiac hypertrophy during chronic arterial vasodilation.