Demonstration that circulating human blood cells have no detectable alpha 1-adrenergic receptors by radioligand binding analysis.

ABSTRACT

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.