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STIMULATION OF SPECIFIC [ 3 H]‐OUABAIN BINDING TO MICROSOMAL PREPARATIONS FROM RAT HEART AND SKELETAL MUSCLE BY THYROID HORMONES: EFFECTS OF 6‐HYDROXYDOPAMINE
Author(s) -
BANERJEE SHAILESH P.,
SHARMA VIRENDRA K.
Publication year - 1979
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1979.tb07872.x
Subject(s) - medicine , endocrinology , skeletal muscle , triiodothyronine , euthyroid , ouabain , denervation , cardiac muscle , chemistry , gastrocnemius muscle , thyroid , hormone , biology , organic chemistry , sodium
1 Surgical thyroidectomy decreased specific [ 3 H]‐ouabain binding to heart ventricular microsomes by 43% and gastrocnemius muscle microsomes by 34%. Administration of triiodothyronine to euthyroid rats enhanced specific [ 3 H]‐ouabain binding to heart and skeletal muscle membrane by 60% and 33% respectively. 2 Treatment of thyroidectomized rats with triiodothyronine increased specific [ 3 H]‐ouabain binding by 44% in skeletal muscle membrane preparation and 428% in cardiac microsomes. 3 Specific [ 3 H]‐ouabain binding decreased by 55% in heart and 53% in gastrocnemius muscle preparations following chemical sympathectomy with 6‐hydroxydopamine. 4 Treatment with triiodothyronine of euthyroid rats which had been sympathectomized did not significantly alter specific [ 3 H]‐ouabain binding to heart or skeletal muscle membrane preparations. 5 Administration of triiodothyronine to thyroidectomized and sympathectomized rats increased specific [ 3 H]‐ouabain binding by 80% in heart and 83% in skeletal muscle membrane preparations. 6 These results suggest that triiodothyronine may influence specific [ 3 H]‐ouabain binding to thyroid hormone nonresponsive tissue such as sympathetic nerve endings. Therefore, the present observations are incompatible with the hypothesis that induction of (Na + 4‐ K + )‐adenosine triphosphatase of skeletal muscle membrane is the molecular mechanism for the calorigenic actions of thyroid hormones.