Failure of neurotransmitter blockers to alter PGE2-induced LH release.
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概要
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The purpose of this study is to ascertain whether or not prostaglandin (PG) E<SUB>2</SUB>induces LH release by modifying or modulating the release or action of neural transmitters.<BR>PGE<SUB>2</SUB>injected iv into spayed rats primed two days earlier with 10βg estradiol benzoate increased the plasma levels of LH 10 min later as measured by radio-immunoassay. The peak of plasma LH was not changed by prior treatment with βorα-adrenergic receptor blockers, propranolol or phenoxybenzamine. The peak level of plasma LH did not alter in rats treated with DL-α-methyl-p-tyrosine methyl ester HCI (α-MPT) or sodium diethyldithiocarbamate (DDC). Similarly, the peak of plasma LH was not changed by prior treatment with imipramine. Administration of PGE<SUB>2</SUB>produced an increase in anlerior pituitary and plasma, but not hypothalamic cyclic AMP concomitantly with the elevation in plasma LH.<BR>Although it is possible that the effect of PGE<SUB>2</SUB>could be mediated by another transmitter system, as yet unknown, or that the effect of PGE<SUB>2</SUB>on LH release could be mediated via the adenylate cyclase-cyclic AMP system, the results indicate that PGE<SUB>2</SUB>does not act trans-synaptically, but probably acts directly on LH-RH neurons.
- 一般社団法人 日本内分泌学会の論文