Pressure-overloaded cardiac hypertrophy was induced by abdominal aortic constriction in 10-week-old male Wistar rats. 24-26 weeks after aortic constriction, the hearts were excised and a myocardial mechanical study was performed using isolated left ventricular papillary muscles. There was no significant difference in isometric developed tension (T) between sham-operated control and aortic constriction (AC) rats (control vs AC rats = 2.9 +/- 0.6 vs 2.7 +/- 0.7 g/mm2). dT/dtmax of AC rats, on the other hand, was significantly lower than that of controls (controls vs AC rats = 32.8 +/- 7.5 vs 26.3 +/- 6.1 g/mm2s, p less than 0.05). Myocardial mechanical responses to isoproterenol (10(-7) mol/l) were depressed in the group with aortic constriction compared with the control group (delta T: 18.5 +/- 6.7 vs 12.1 +/- 4.9%, p less than 0.05, delta dT/dt: 25.2 +/- 6.2 vs 17.5 +/- 5.8%, p less than 0.02). Responses of the parameters to dibutyryl cyclic AMP (10(-5) mol/l) were also smaller in the AC group than in the control group (delta T: 18.0 +/- 5.6 vs 13.3 +/- 4.0%, p less than 0.05, delta dT/dt: 20.4 +/- 6.9 vs 14.7 +/- 4.1%, p less than 0.05). Left ventricular myosin isoenzyme pattern, revealed by pyrophosphate gel electrophoresis, shifted towards VM-3 under pressure overload. The present study demonstrates that post-membrane processes may be mainly responsible for the decreased myocardial mechanical catecholamine responsiveness in pressure-overloaded cardiac hypertrophy.