Gewählte Publikation:
Porta, S; Ertl, U; Nauman, J; Nauman, A; Rinner, I; Fiedorowicz, K.
Decrease of rat-liver-T4-5'-deiodinase activity during chronical isoprenaline beta-action in vivo.
EXP PATHOL. 1987; 31(3): 179-183.
Doi: 10.1016/S0232-1513(87)80106-8
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Porta Sepp
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- Abstract:
- Pure adrenergic beta-action, brought about by long-term adrenaline + regitine application in rats, was able to increase liver T4-5'-deiodinase activity for 8 h (Nauman et al. 1984a). Long-term isoprenaline application without alpha-blocking yielded contrary results. One of the compensatory mechanism to be probably blamed could have been the very high endogenous adrenaline-levels (Porta et al. 1985). Simultaneous treatment with isoprenaline and alpha-methyltyrosinemethylester did not settle the problem since even then deiodinase activity was still drastically decreased. Two more components have been found which could very well be the reason for that "paradox beta-action" in vivo, namely very low glucose and insulin levels, both of which are known to influence deiodinase activity. In vivo--contrary to in vitro--it is seemingly not possible that catecholaminergic beta-action could increase the peripheral production of T3 unless general alpha-blocking took place.
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Animals -
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Blood Glucose - metabolism
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Insulin - blood
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Iodide Peroxidase - metabolism
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Liver - drug effects
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Male - drug effects
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Methyltyrosines - pharmacology
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Rats - metabolism
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Rats, Inbred Strains - metabolism
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Receptors, Adrenergic, beta - drug effects
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Time Factors - drug effects