Left ventricular adaptation to gradual renovascular hypertension in dogs

The left ventricle hypertrophies in response to chronic pressure overload. To determine whether increased beta-adrenergic stimulation, wall mass, intrinsic contractility, or a combination of these factors is responsible for improved left ventricular (LV) pump function during early development of pressure-overload hypertrophy and whether hypertrophy normalizes peak-systolic wall stress, as is commonly believed, we induced pressure overload in intact-chest dogs by gradual constriction of one renal artery and implanted radiopaque markers, via a catheter, in the LV endocardium to measure dimensions. Changes in hemodynamics, LV dimensions, contractility indexes, and circumferential wall stress were measured before and after acute beta-blockade for 12 wk. LV function improved over time in the unblocked state, indicated by increased cardiac output, systolic pressures, stroke work, and maximal elastance (Emax). Acute beta-blockade reduced stroke work, Emax, and maximal LV rate of pressure over time (dP/dtmax) relative to the unblocked state but all still increased significantly over time. dP/dtmax and Emax did not vary with increases in LV mass, but stroke work was borderline dependent on LV mass. These results suggest that beta-adrenergic stimulation contributes to improved LV pump function and that the remaining improvements are due to both increased intrinsic contractility and wall mass. In contrast to accepted theory, LV systolic wall stresses decreased significantly over time. End-diastolic wall stress increased after renal artery constriction, then returned to baseline values as the heart hypertrophied. These results suggest that hypertrophy normalizes end-diastolic, not peak-systolic, wall stress.