1. This study was done to characterize the functional role of alpha 1D-adrenoceptors in rat myocardium, aorta, spleen, vas deferens and prostate by use of the selective antagonist BMY 7378. 2. BMY 7378 inhibited [3H]-prazosin binding to aortic membranes with a potency (pKi 9.8+/-0.40) approximately 100 fold higher than in right ventricular membranes (pKi 7.47+/-0.11) and approximately 1,000 fold higher than that in plasma membranes of the prostate (pKi 6.62+/-0.39), vas deferens (pKi 6.67+/-0.15), salivary gland (pKi 6.46+/-0.38) and liver (6.58+/-0.06). 3. BMY 7378 antagonized the positive inotropic effects of phenylephrine (in the presence of 1 microM propranolol) on right ventricles (pA2 7.0+/-0.11), left atria (pKB 7.04+/-0.18) and papillary muscles (pKB 6.9+/-0.1) and inhibited phenylephrine-induced increase in inositol phosphates. 4. BMY 7378 was approximately 100 fold more potent as an antagonist of phenylephrine on aortic strips (pA2 9.0+/-0.13) than on vas deferens (pKB 7.17+/-0.08) and spleen (pKB 7.16+/-0.21); it was ineffective on the prostate. 5. Chloroethylclonidine suppressed the maximal effects of phenylephrine on spleen; 5-methylurapidil antagonized the effects of phenylephrine on aortic strips (pA2 7.98+/-0.08), vas deferens (pKB 8.89+/-0.07) and prostate (pKB 8.85+/-0.21). 6. BMY 7378 caused a dose (0.1-100 nmol kg-1)-dependent decrease in mean blood pressure of urethane-anaesthetized rats and its hypotensive efficacy was equal to that of hexamethonium. 7. The data suggest that alpha 1D-adrenoceptors play a significant role in rat aorta, a minor role in the heart, vas deferens and spleen and virtually no role in the prostate.