AJP - Heart and Circulatory Physiology, Vol 256, Issue 3 876-H880, Copyright © 1989 by American Physiological Society
Arterial vasodilators, cardiac volume load, and cardiac hypertrophy in normotensive rats
J. Tsoporis, B. X. Yuan and F. H. Leenen
Division of Clinical Pharmacology, Toronto Western Hospital, Ontario, Canada.
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.
