The aim of the study was to investigate the role of the α 1D-adrenoceptor in α1D-adrenoceptor-induced contraction of human prostate by means of protection experiments. Responses of human prostate strips to noradrenaline were recorded, along with responses of rat aorta and vas deferens, tissues possessing predominantly α 1D and α1A-adrenoceptors respectively, for comparison. α1D-adrenoceptors were then inactivated by incubation with the irreversible antagonist phenoxybenzamine. In some tissues α1A- or α1D-adrenoceptors were 'protected' from inactivation by incubation in the presence of the selective α 1A- or α1D-adrenoceptor antagonists 5-methylurapidil and BMY 7378 before recording further responses to noradrenaline. Phenoxybenzamine reduced the maximum noradrenaline-induced response and the potency of noradrenaline in all tissues. In rat vas deferens and human prostate, 5-methylurapidil protected α 1A-adrenoceptors in a concentration-dependent manner. In rat aorta, 10 nM BMY 7378 almost fully protected α1D-adrenoceptors. However, concentrations of BMY 7378 up to 30-fold higher failed to protect receptors in the human prostate. These results suggest that in human prostate functional α1D-adrenoceptors do not contribute to noradrenaline-induced contractile responses.