The direct cardiac effects of hydralazine were studied in isolated working rat heart, isolated cat right ventricular papillary muscle, and isolated rabbit right atrium. The haemodynamics, myocardial energetics, and contractility of isolated hearts were measured at hydralazine concentrations of 0.01, 0.1, 0.5, 1.0, 10 and 100 mumol.litre-1. Coronary flow was significantly increased (greater than or equal to 21%, p less than 0.01) in paced (325 beats.min-1) rat hearts at greater than or equal to 0.5 mumol.litre-1 hydralazine and in spontaneously beating hearts (greater than or equal to 37%; p less than 0.05) at greater than or equal to 1.0 mumol.litre-1 hydralazine. The increases in coronary flow occurred without significant increases in heart rate, contractility (dP/dtmax), or coronary perfusion pressure. Myocardial oxygen consumption was not significantly changed at any hydralazine concentration in spontaneously beating hearts and was unaltered in paced hearts except for a small significant increase (9.8%) at 10 mumol.litre-1. A negative inotropic effect was apparent at 100 mumol.litre-1 hydralazine as indicated by a significant reduction of dP/dtmax (paced and non-paced hearts), peak aortic flow rate (non-paced), and maximum left ventricular pressure (paced). In isolated cat papillary muscles and rabbit right atria, cumulative hydralazine log dose-response curves (0.1-1000 mumol.litre-1) were obtained. A positive inotropic effect that could be abolished by beta adrenergic blockade was produced in papillary muscles only at concentrations greater than or equal to 100 mumol.litre-1.(ABSTRACT TRUNCATED AT 250 WORDS)