title: Influence of thyroid status on intracellular distribution of cardiac adrenoceptors.
abstract: Previous studies have suggested that thyroid hormones influence the number of membrane-bound cardiac adrenoceptors, but their effect on the intracellular distribution of adrenoceptors has not been examined. A plasma cell membrane and a vesicular fraction devoid of membrane markers were prepared from hearts of euthyroid and hyperthyroid rats and were used to compare beta- and alpha-adrenoceptors. During daily injection of l-thyroxine, cardiac hypertrophy developed within 4 days and remained unchanged thereafter. The number of membrane-bound beta-receptors increased progressively and plateaued within 2 weeks of thyroxine administration. Vesicular beta-receptors, on the other hand, increased more gradually and to a lesser extent so that after 2 weeks of l-thyroxine injection, they constituted a smaller proportion of the total beta-receptor population compared to normal rats. In contrast, the number of cardiac alpha 1-adrenoceptors declined rapidly to about 80% of that in euthyroid animals and did not change further for the duration of the study. Membrane-bound and vesicular alpha 1-adrenoceptors were affected to the same extent in hyperthyroidism. During regression of cardiac hypertrophy following cessation of thyroxine administration, alpha 1-adrenoceptors rose rapidly (within 2 days) to normal values while beta-receptors declined more gradually to normal levels within 2 weeks. In hypothyroid rats, there was a significant decline in the density of both alpha 1- and beta-adrenoceptors, with a shift away from the vesicular fraction. These results indicate that both the total numbers of cardiac adrenoceptors and their distribution between the plasma membrane and vesicular fraction are influenced by the thyroid status.
authors.affiliation: Department of Laboratory Medicine, University of Minnesota School of Medicine, Minneapolis.
authors.forename: C
authors.initials: C
authors.lastname: Limas
authors.forename: C J
authors.initials: CJ
authors.lastname: Limas
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000139:chemically induced / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D004082:Dihydroalprenolol / Q000378:metabolism; D006980:Hyperthyroidism / Q000139:chemically induced / Q000378:metabolism; D007037:Hypothyroidism / Q000139:chemically induced / Q000378:metabolism; D007700:Kinetics; D008297:Male; D008713:Methimazole; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D011942:Receptors, Adrenergic, alpha / Q000378:metabolism*; D011943:Receptors, Adrenergic, beta / Q000378:metabolism*; D013963:Thyroid Hormones / Q000502:physiology*; D013974:Thyroxine
chemical_list: D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; D013963:Thyroid Hormones; D008713:Methimazole; D004082:Dihydroalprenolol; D013974:Thyroxine