AJP - Endocrinology and Metabolism, Vol 262, Issue 4 E504-E510, Copyright © 1992 by American Physiological Society

ARTICLES

Skeletal muscle beta-adrenoceptor distribution and responses to isoproterenol in hyperthyroidism

W. H. Martin 3rd, E. Korte, T. K. Tolley and J. E. Saffitz
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.

To determine whether hyperthyroidism selectively increases beta-adrenergic receptor density in vessels or fibers of human skeletal muscle, we characterized beta-receptor distribution autoradiographically in muscle biopsies of 18 subjects aged 26 +/- 1 yr before and after daily administration of 100 micrograms 3,5,3'-triiodothyronine (T3) for 2 wk. To establish whether vascular and metabolic responses to beta-adrenergic stimulation are concomitantly altered, we quantified calf blood flow and plasma concentrations of glucose, lactate, glycerol, free fatty acids (FFA), insulin, and C-peptide during graded-dose isoproterenol infusion in eight of these individuals. Differences in beta-adrenergic receptor density among muscle fiber types and vascular components were highly significant (type I greater than type IIa greater than type IIb muscle fibers, P less than 0.001; and type I muscle fibers greater than resistance arterioles, P less than 0.05). Hyperthyroidism increased beta-adrenergic receptor density in all types of muscle fibers (+31-50%; P less than 0.01) but not in resistance arterioles. There was no change in calf blood flow or plasma glucose, glycerol, FFA, insulin, or C-peptide responses to isoproterenol. A rise in lactate during stages 3 and 4 of isoproterenol infusion (P less than 0.01) was observed before but not after T3 administration. Thus hyperthyroidism increases beta-adrenergic receptor density in fibers but not vessels of human skeletal muscle without increasing either metabolic or vascular responses to selective beta-adrenergic stimulation.

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