The highly specific alpha 2-adrenoceptor antagonist 3H-yohimbine was used to label in guinea-pig kidney and calf cerebral cortex membranes alpha 2-adrenoceptors. In both tissues binding was saturable, of high affinity (KD = 3-5 nM), rapid and readily reversible. alpha-Adrenergic antagonists inhibited binding with rank order of potency: rauwolscine greater than or equal to yohimbine greater than phentolamine much greater than prazosin greater than or equal to corynanthine, which is the typical one for alpha 2-adrenoceptors. Displacement curves of alpha-adrenergic agonists (clonidine greater than guanfacine greater than adrenaline greater than or equal to noradrenaline) were in the absence of GTP shallow with pseudo-Hill coefficients (nH) significantly less than 1.0. In the presence of GTP (10(-4) M) the curves were shifted to the right to lower affinities. However, only in guinea-pig kidney membranes nH increased up to 1.0, while in calf cerebral cortex membranes nH was not significantly influenced by GTP. The properties of alpha 2-adrenoceptors--as assessed by 3H-yohimbine binding--in guinea-pig kidney and calf cerebral cortex are, therefore, very similar to those recently determined under identical experimental conditions in human platelet membranes (Brodde et al., 1982). Although some tissue and/or species differences exist--especially the 5-6 times higher affinity of prazosin at renal and brain than at platelet alpha 2-adrenoceptors--it is concluded that alterations of human platelet alpha 2-adrenoceptors under various (patho) physiological conditions can be taken as representative for changes of other peripheral and/or central alpha 2-adrenoceptors.