The effects of diltiazem treatment (40–50 mg/kg/day orally for 8 weeks) of left ventricular hypertrophy on systemic and coronary hemodynamics and mechanical cardiac performance were investigated in renovascular hypertensive rats (Goldblatt, two-kidney, one clip). Systemic and coronary hemodynamics were determined by using radioactive microspheres in conscious, unrestrained rats. Mechanical performance was measured on isolated papillary muscle from the same animal. Nine treated hypertensive rats were compared with control groups: 12 untreated hypertensive and nine sham-operated rats. Diltiazem treatment led to an effective but incomplete control of blood pressure (from 208 ± 5 mm Hg in the untreated hypertensive group to 155 ± 3 mm Hg in the treated hypertensive group; p < 0.01) associated with a significant but incomplete decrease of the left ventricular mass (from 3.10 ± 0.19 mg/g in untreated hypertensive rats to 2.35 ± 0.04 mg/g in treated hypertensive rats; p < 0.01). A close correlation was found between left ventricular mass and systolic blood pressure in untreated, treated, and pooled groups (r=0.84, p < 0.001, n=30). The left ventricular weight to systolic blood pressure ratio was equivalent in all three groups, so that the reduction of left ventricular mass in diltiazem-treated rats was commensurate with the reduction of blood pressure. At rest, treated hypertensive rats showed a rise in cardiac output (426 ± 12 vs 298 ± 22 ml/min/kg in sham-operated rats; p < 0.001) and in coronary blood flow (598 ± 17 vs 453 ± 19 ml/min/100 g; p < 0.05) related to the decrease in total peripheral resistance and in total left ventricular coronary resistance. A reversal of impaired myocardial mechanical parameters toward control values was observed except for time to half-maximal relaxation (92 ± 2 msec in the treated group vs 79 ± 5 msec in sham-operated rats) and time to peak force. Our results demonstrate that even incomplete control of blood pressure with diltiazem is associated with significant but partial reduction of left ventricular mass and improvement of mechanical function.