To investigate if anti-hypertensive drug therapy is effective in correcting the altered endo-thelial responses observed in blood vessels of DOCA-salt hypertensive rats, cumulative concentration-effect curves to noradrenaline, acetylcholine and sodium nitroprusside were constructed in rings of thoracic aortas with or without endothelium isolated from DOCA-salt hypertensive and control rats treated with hydralazine for 24 h (acute) or 15 d (chronic). Effective concentrations (EC50s) and maximal responses were analysed. Blood pressures of both control and DOCA-salt hypertensive rats decreased within 24 h to levels at or below those obtained before treatment and were maintained at reduced levels during the remainder of the treatment period (15 d). In preparations with endothelium, lower EC50s for noradrenaline were observed in aortas from DOCA-salt hypertensive rats in comparison with corresponding controls except for hydralazine (15 d) -treated group. The maximal responses to noradrenaline did not differ significantly between the different groups Similar EC50s and maximal responses to noradrenaline were observed in preparations without endothelium from DOCA-salt hypertensive and corresponding control rats. After acute and chronic hydralazine treatment similar responses to acetylcholine were found. An increased sensitivity to sodium nitroprusside, an endothelium-independent vasodilator, was found 15 days after hydralazine treatment. We concluded that: a) the increased sensitivity to noradrenaline observed in aortic rings with endothelium from DOCA-salt hypertensive rats was not corrected by acute treatment; chronically administered hydralazine potentiated noradrenaline responses in control aortas, therefore it was not possible to conclude about the influence of the anti-hypertensive treatment on the potentiated response observed in hypertensive aortas; b) acute and chronic hydralazine treatments corrected the impaired endothelium-dependent relaxation observed in aortas of DOCA-salt hypertensive rats; c) acute hydralazine treatment did not alter the relaxing response of smooth muscle in DOCA-salt rats; however, the chronic treatment increased the sensitivity to sodium nitroprusside in aortas of DOCA-salt rats. Therefore, correction of the decreased response to acetylcholine might, at least partially, be due to an increased response of vascular smooth muscle to nitrovasodilators such as NO that is released by acetylcholine.