The main purpose was to assess the existence of alpha 2-adrenoceptors in isolated segments of the proximal portion of the rat tail artery. Adrenaline and phenylephrine evoked strong contractile responses, whereas in 22 out of 49 arteries, 10-100 microM clonidine evoked weak contractions. Guanabenz, idazoxan and yohimbine lacked contractile effects. Reserpine pretreatment did not modify the percentage of responsive arteries to clonidine nor the ineffectiveness of guanabenz. Raising the Ca2+ concentration to 2.5 mM did not alter the responsiveness to adrenaline and phenylephrine but enhanced the amplitude of the responses to clonidine. The exposure to 0.1 or 1.0 microM angiotensin did not affect the responsiveness to clonidine. Responses to clonidine were abolished by 10 nM prazosin and not affected by 1 microM idazoxan or yohimbine. Adrenaline and phenylephrine concentration-response curves were shifted rightward by prazosin and phentolamine (pA2 within 7.3-9.0) and by clonidine, guanabenz, idazoxan and yohimbine (pA2 lower than 6.5). These data suggest that the tail artery lacks postsynaptic alpha 2-adrenoceptors, that clonidine exerts partial alpha 1-agonist/antagonist effects and that guanabenz, idazoxan and yohimbine act as partial alpha 1-antagonists.