The interaction of the beta-blocker tertatolol with the prejunctional beta-adrenoceptors of the rat renal vasculature was examined. In isolated Tyrode-perfused rat kidneys isoproterenol (5 x 10(-7) M to 2 x 10(-6) M) slightly decreased the pressor responses to noradrenaline (0.5 nmol), but markedly increased those to electrical stimulation (6 Hz). Tertatolol at 3 x 10(-7) M inhibited both effects of isoproterenol. Electrical stimulation (6 Hz) caused an overflow of intact 3H-noradrenaline from kidneys previously labelled with the 3H-transmitter; this stimulation-induced release was augmented by isoproterenol. Also this effect of isoproterenol was prevented by 3 x 10(-7) M of tertatolol. In different groups of rat kidneys labelled with 3H-noradrenaline, isoproterenol (5 x 10(-7) M) augmented the stimulation (1 Hz), induced 3H overflow and this increased transmitter output was concentration-dependently inhibited by tertatolol and propranolol; from the IC50 values it was calculated that tertatolol was 16 times more potent than propranolol. Even at concentrations up to 10(-5) M, neither tertatolol nor propranolol significantly altered the basal and stimulation-induced transmitter release from the rat kidneys. From the data we conclude that tertatolol is a powerful inhibitor of the prejunctional beta-adrenoceptors in the renal circulation of the rat. Stimulation of these receptors by beta-agonists not only enhances transmitter release but also increases the pressor responses induced by electrical stimulation.