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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Heterogeneity of alpha 1-adrenergic receptors revealed by chlorethylclonidine.

Chlorethylclonidine (CEC) has previously been shown to inactivate only a subpopulation of the alpha 1-adrenergic receptor binding sites in rat brain. We compared alpha 1-adrenergic receptors in different tissues to determine whether such selective inactivation might reveal the presence of distinct receptor subtypes. Pretreatment of broken cell preparations with 10 microM CEC for 10 min caused a 70-80% decrease in the density of specific 125IBE 2254 binding sites in rat liver and spleen, a 25% decrease in neocortex, but no significant loss in kidney, hippocampus, heart, vas deferens, or caudal artery. The effect of CEC in liver was not reversed by extensive washing, suggesting irreversible inactivation. The selectivity between different tissues was due to differences in the efficacy of CEC inactivating the binding sites and not due to differences in binding affinity. To determine whether the effects on 125IBE 2254 binding reflected selective inactivation of functional receptors, contractile responses of rat spleen and vas deferens were examined. Pretreatment of intact tissues with 100 microM CEC for 30 min caused a large decrease in the potency and maximal contraction to norepinephrine in spleen but had no effect in vas deferens. Inhibition of specific 125IBE 2254 binding by various agonists and antagonists was determined in CEC-sensitive (liver, spleen) and insensitive (hippocampus, vas deferens) tissues. Although many drugs had similar affinities in all tissues, others were substantially less potent in the CEC-sensitive tissues. These experiments suggest that there are at least two subtypes of alpha 1-adrenergic receptors with different pharmacological properties in mammalian tissues, only one of which is inactivated by CEC.[1]


  1. Heterogeneity of alpha 1-adrenergic receptors revealed by chlorethylclonidine. Han, C., Abel, P.W., Minneman, K.P. Mol. Pharmacol. (1987) [Pubmed]
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