Coronary blood flow in senescent rats with late-onset hypertension.

We tested the hypothesis that the imposition of hypertension late in life would markedly limit maximal myocardial perfusion (MP). Young adult (8 mo) and senescent (24 mo) Fischer 344 rats were studied 3 mo after one-kidney, figure-8 renal wrap hypertension (RH) was induced. Sham-operated rats served as controls (Con). Regional MP was determined with radioactive microspheres in conscious rats before and during maximal coronary vasodilation with infusion of dipyridamole. Systolic arterial pressure (SAP) was significantly elevated in both RH age groups during weeks 2-6 following surgery and then fell to normotensive levels. After 3 mo SAP (mmHg) was significantly lower in the senescent RH rats (125 +/- 5) compared with their controls (147 +/- 3). In senescent RH rats left ventricular (LV) end-diastolic pressure increased fivefold. LV mass increased with age but not with treatment. LV minimal coronary vascular resistance (MCVR, mmHg.ml-1.min-100 g) increased significantly both with age and treatment (8 mo: Con = 0.07 +/- 0.01, RH = 0.14 +/- 0.01; 24 mo: Con = 0.11 +/- 0.01, RH 0.17 +/- 0.02). Treatment affected similar changes in the right ventricular MCVR. LV endocardial-to-epicardial perfusion ratio during rest was lower in the senescent groups but was not altered by hypertension. These data indicate that 1) both aging and this model of hypertension compromise maximal coronary perfusion and reserve in Fischer 344 rats, and 2) aging is associated with an increase in coronary vascular resistance in both ventricles at rest and in a relative reduction in maximal endocardial perfusion in the left ventricle.