4 ホルモン作用と標的細胞呼吸代謝系の応答 : 甲状腺刺激ホルモンと副甲状腺ホルモンの作用機序についての考察
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In an attempt to elucidate the mode of hormone action in the most physiological situations, an <I>in vivo</I>-<I>in vivo</I> system (hormone was introduced <I>in vivo</I>, and the resulting biochemical responses were examined also <I>in vivo</I>) was studied by the use of an organ-microfluorometer. The instrument, developed by our hands for these particular ends, permits a faithful monitoring of alterations in the intracellular redox state of organs <I>in situ</I>, by continuously recording the fluorescence signal from reduced pyridine nucleotides which is compensated for the "hemodynamic artifact". As examples of the study were presented the effect of thyrotropin and that of parathyroid hormone.<BR>1. Thyrotropin (Thytropar, Armour) given iv to thyroxine-treated rabbits and rats caused a prompt and sustained fall in the level of reduced pyridine nucleotides in thyroid. Bovine serum albumin, growth hormone, prolactin, parathyroid hormone, luteinizing hormone, and follicle stimulating hormone did not reproduce the thyrotropin effect. Thyrotropin did not affect kidney, testis, or parathyroid pyridine nucleotides. Such oxidative shift of thyroid redox-sta te of pyridine nucleotides as produced by thyrotropin was mimicked by Dicoumarol or by long-acting thyroid stimulator. 3′, 5′-cyclic AMP or dibutyryl cyclic AMP, on the other hand, led to a reductive shift of the thyroid redoxstate. From these results a possibility is discussed that thyrotropin in vivo acts on thyroid to result, independently of the adenyl cyclase activation, in the oxidation of reduced pyridine nucleotides.<BR>2. A parathyroid extract (Parathormone, Lilly) injected iv to rats induced a prompt and transient reduction in the kidney. This action was mimicked by calcium salts of poorly membrane-permeant anion like dextran-sulfate. Calcium salts of apparently permeant anion (e.g., aspartate) as well as EDTA or EGTA produced an oxidative response. The transient reduction was also reproduced by giving reductive substrates of the cytosol dehydrogenases. These results led to a hypothesis that parathyroid hormone causes a rise in the calcium ion activity in the cytosol compartment of renal tubules, resulting somehow in an accelerated production of the reductive substrate (s).
- 日本内分泌学会の論文
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