Zhu S J, Toews M L
Department of Pharmacology, University of Nebraska Medical Center, Omaha.
J Pharmacol Exp Ther. 1993 Oct;267(1):123-7.
Depletion of intracellular ATP with antimycin A has been shown to inhibit the internalization of several types of receptors, including beta adrenergic and muscarinic acetylcholine receptors. The effects of antimycin A treatment on conversion of beta and alpha-1 adrenergic receptors to a form exhibiting low apparent affinity for agonists in assays with intact cells were investigated, because conversion to the low-affinity form has been postulated to result from receptor internalization. Treatment of DDT1 MF-2 hamster smooth muscle cells with antimycin A greatly decreased conversion of beta adrenergic receptors to the form exhibiting low affinity for agonists. Binding of antagonists to intact cell beta adrenergic receptors was not altered by antimycin A. In contrast to the results with beta adrenergic receptors, conversion of alpha-1 adrenergic receptors to the low-affinity form was not inhibited by antimycin A. These results are consistent with the possible involvement of receptor internalization in conversion to the low affinity form for beta adrenergic receptors. They also provide further evidence that different mechanisms may be involved in conversion to the low-affinity form or in the internalization pathway in the case of alpha-1 adrenergic receptors.
