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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 316 (1981), S. 45-50 
    ISSN: 1432-1912
    Keywords: Rat cerebral cortex ; α1-Adrenoceptor ; [3H]-WB4101 binding ; Hyperthyroidism ; Hypothyroidism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of thyroid hormones on the concentration and properties of α1-adrenoceptors in a crude membrane fraction obtained from the rat cerebral cortex was investigated using the [3H]-WB 4101 binding assay. Animals were made hypothyroid by feeding 6-propyl-2-thiouracil for 8 weeks. Hyperthyroidism was induced by triiodothyronine injections (50 μg/100 g body weight) for 9 days. 1. The binding of [3H]-WB 4101 was saturable and of high affinity in controls as well as in hyper- and hypothyroid animals. The maximal number of binding sites (B max), which amounted to 95 fmol/mg protein in control animals, was increased by 27% in cortical membranes from hyperthyroid rats and reduced by 23% in the hypothyroid group. 2. The reduction in [3H]-WB 4101 binding due to 6-propyl-2-thiouracil feeding was reversible by triiodothyronine treatment. 3. Dissociation constants (K D) calculated from saturation experiments (0.25 nM) or kinetic data (0.21 nM) remained unchanged in altered thyroid states. 4. Inhibition of [3H]-WB 4101 binding by adrenergic agonists and antagonists revealed no differences between euthyroid and hypothyroid animals. The higher affinity of prazosin to the binding sites compared with yohimbine indicated that [3H]-WB 4101 predominantly labeled α1-adrenoceptors. It is concluded that thyroid hormones regulate the number of α1-adrenoceptors in membranes of the rat cerebral cortex, leaving their affinities unchanged.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 317 (1981), S. 159-164 
    ISSN: 1432-1912
    Keywords: Pithed rat ; Hypothyroidism ; Hyperthyroidism ; Plasma catecholamines ; Circulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Altered thyroid states are known to produce profound changes in sympathetic mechanisms. The influence of thyroid hormones on plasma catecholamines, adrenal catecholamines and on circulatory parameters were studied in pithed rats. Animals were made hypothyroid by feeding 6-propyl-2-thiouracil for 6 weeks. Hyperthyroidism was induced by triiodothyronine injections (0.5 mg/kg body weight) for 7 days. 1. The basal heart rate was decreased in hypothyroidism and accelerated in hyperthyroidism. Basal diastolic blood pressure was reduced in both dysthyroid states. 2. Electrical stimulation of autonomic outflow from the spinal cord induced tachycardia and increased diastolic blood pressure. The increase in heart rate due to electrical stimulation was reduced in hypo- and hyperthyroidism. In hyperthyroid animals this may be due to the already accelerated basal heart rate. The initial rise in diastolic blood pressure was decreased in the hypothyroid and increased in the hyperthyroid state. 3. Basal adrenaline plasma levels were higher than control values in hypothyroidism and unaltered in hyperthyroidism. Basal noradrenaline levels were not significantly influenced by either thyroid state. 4. The increase in plasma noradrenaline during electrical stimulation was enhanced in hyperthyroid animals and remained unaltered by hypothyroidism. 5. The increase in plasma adrenaline during electrical stimulation was significantly changed in both dysthyroid states. Hyperthyroidism reduced the initial peak of adrenaline release. Hypothyroidism raised plasma adrenaline in the steady state after sustained stimulation. 6. Elevated basal and stimulated adrenaline plasma levels corresponded to an increased adrenaline content and enhanced phenylethanolamine-N-methyltransferase activity in adrenal glands of hypothyroid rats. The significant influence of thyroid hormones on plasma catecholamines seems to contribute but cannot explain completely the circulatory changes in hypo- and hyperthyroidism. The role of additional factors such as receptor changes and central nervous mechanisms is discussed.
    Type of Medium: Electronic Resource
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