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Myocardial and Vascular Structural Adaptation to Chronic Pressure Overload

Left ventricular (LV) function and end-diastolic dimensions were determined during antegrade and retrograde perfusions, respectively. Isolated hearts from spontaneously hypertensive rats (SHRs) and renal hypertensive rats and SHRs to which either feldopine, nifedipine, α-methyldopa, or a combination of felodipine and metoprolol was administered were used. Maximal cardiac function [cardiac output × (aortic pressure - left atrial pressure)] was elevated in SHRs, but depressed in those with renal hypertension. The diastolic pressure-volume relationships revealed eccentric rather than concentric LV hypertrophy in the SHRs. Renal hypertension in SHRs caused concentric LV hypertrophy. Antihypertensive therapy with calcium antagonists (but not with α-methyldopa) caused reduction of LV wall thickness, but increased LV end-diastolic volume (EDV). In SHRs, coronary flow was reduced at any given level of aortic pressure. At low aortic pressures (and hence, limited coronary perfusion), cardiac function was attenuated in SHRs. This reduction could be reversed by administration of antihypertensive therapy. These results suggest an improvement in maximal stroke work in SHRs as a result of eccentric hypertrophy which allows increased stroke volume for a given degree of myocardial shortening. Structural coronary vascular changes, which can be reversed by antihypertensive therapy, can limit coronary perfusion—and hence, cardiac performance—at low aortic pressures in SHRs. Maintenance of maximal cardiac function in treated SHRs, despite a reduction in LV wall thickness, may be due to an increase in LV end-diastolic volume.