RESUMO
The mechanisms underlying the autonomic nervous system abnormalities reported in allergic asthma have not been defined. In order to determine if these abnormalities reflect abnormal alpha-adrenergic receptor numbers or drug affinities, we attempted to identify alpha-receptors on circulating human blood cells. Platelets, red blood cells, polymorphonuclear leukocytes, and mononuclear cells were examined by use of radioligand binding techniques with the [3H]antagonists, dihydro-alpha-ergocryptine, prazosin hydrochloride, and yohimbine as ligands. The presence of alpha 2-receptors was confirmed on platelets, but no detectable alpha-receptors were identified on red blood cells or polymorphonuclear leukocytes. Preliminary observations suggested the presence of specific alpha-receptor binding to mononuclear cells; however, this binding was determined to reflect directly the presence of contaminating platelets. By use of a newly developed isolation technique to obtain platelet-depleted mononuclear cells, no alpha-adrenergic receptors could be identified on platelet-depleted mononuclear cells. Therefore, since no alpha 1-receptors could be identified on circulating human blood cells, these cells are not a suitable model for the study of the mechanisms underlying abnormal alpha-adrenergic responsiveness, and it may be necessary to reanalyze previous reports of alpha-adrenergic responsiveness on human blood cells with the use of platelet-depleted cell preparations.