Original article
Demonstration that circulating human blood cells have no detectable alpha1-adrenergic receptors by radioligand binding analysis

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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 α-adrenergic receptor numbers or drug affinities, we attempted to identify α-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-α-ergocryptine, prazosin hydrochloride, and yohimbine as ligands. The presence of α2-receptors was confirmed on platelets, but no detectable α-receptors were identified on red blood cells or polymorphonuclear leukocytes. Preliminary observations suggested the presence of specific α-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 α-adrenergic receptors could be identified on platelet-depleted mononuclear cells. Therefore, since no α1-receptors could be identified on circulating human blood cells, these cells are not a suitable model for the study of the mechanisms underlying abnormal α-adrenergic responsiveness, and it may be necessary to reanalyze previous reports of α-adrenergic responsiveness on human blood cells with the use of platelet-depleted cell preparations.

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    Present address: Dept. of Internal Medicine, U. of Iowa Hospitals and Clinics, Iowa City, IA 52242.

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