dihydroergotoxine has been researched along with Hyperthyroidism* in 3 studies
3 other study(ies) available for dihydroergotoxine and Hyperthyroidism
| Article | Year |
|---|---|
Changes in adrenoreceptor density in brown adipose tissue from hyperthyroid rats.
Treatment of rats with triiodothyronine (T3 10 micrograms/100 g per day, 20 days) increased the mass of brown adipose tissue (BAT) and heart ventricle and stimulated beta-adrenoreceptor number (assessed from radioligand binding) by 43% in isolated BAT and heart membranes. alpha-Receptor number was slightly increased in BAT membranes (42%) but reduced in heart from T3-treated rats. The ratio of alpha-receptors/beta-receptors was unaffected by T3 treatment in BAT membranes (control and hyperthyroid = 1.54) but reduced in heart (control = 2.8, T3 = 1.04). Topics: Adipose Tissue, Brown; Animals; Dihydroalprenolol; Dihydroergotoxine; Hyperthyroidism; In Vitro Techniques; Male; Rats; Rats, Inbred Strains; Receptors, Adrenergic, alpha; Receptors, Adrenergic, beta | 1985 |
White fat cell alpha-adrenergic receptors and responsiveness in altered thyroid status.
Topics: Adipose Tissue; Animals; Cell Membrane; Cricetinae; Cyclic AMP; Dihydroergotoxine; Hyperthyroidism; Hypothyroidism; Kinetics; Male; Mesocricetus; Receptors, Adrenergic; Receptors, Adrenergic, alpha; Thyroid Gland; Thyroxine; Triiodothyronine | 1980 |
Hormone action at the membrane level. VIII. Adrenergic receptors in rat heart and adipocytes and their modulation by thyroxine.
The regulation of adrenergic receptors in rat heart was measured in rats made hyperthyroid by injection with thyroxine and made hypothyroid by addition of propylthiouracil to the drinking water. Hyperthyroid rats display cardiac hypertrophy and a decrease in epididymal fat pad weight. The maximal beta-receptor level of ventricular membranes, as determined by (-)-[3H]dihydroalprenolol binding, was increased 60% by thyroxine treatment and decreased about 30% by propylthiouracil treatment. The affinity of the beta receptor was unchanged after thyroxine or propylthiouracil treatment. The maximal activity of the isoproterenol-stimulated adenylate cyclase (EC 4.6.1.1) varied with thyroid state in a manner parallel to the increase in beta-adrenergic binding sites. Thyroxine treatment also increases by 2-fold the beta receptors in isolated rat fat cells. Propylthiouracil treatment lowered the level of alpha receptors in heart by 30% as measured by [3H]dihydroergocryptine binding, but increased the affinity about 2.5-fold. The highest level of alpha receptors was seen in control hearts. These studies indicate that thyroxine may control the turnover of beta-adrenergic receptors in heart and fat cells and regulate physiological responses in these tissues via a hormone-hormone interplay system. Thyroxine treatment reduced the activity of the membrane-bound Mg2+-ATPase (EC 3.6.1.3) and 5'-mononucleotidase (EC 3.1.3.5) but appears to increase the activity of the (Na+ + K+)ATPase (EC 3.6.1.4). Topics: Adenosine Triphosphatases; Adenylyl Cyclases; Adipose Tissue; Alprenolol; Animals; Cell Membrane; Dihydroergotoxine; Heart; Hyperthyroidism; Hypothyroidism; Male; Propylthiouracil; Rats; Receptors, Adrenergic; Sympathomimetics; Thyroxine | 1978 |