Biomedical subjects
Publications and source records attributed to C Rivier.
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LRF and one of its highly potent analogs, [D-Trp6-Pro9-NEt]LRF (A), were tested for their effects on pregnancy. Daily doses of A prevented implantation and/or caused resorption of implanted blastocysts in mated female rats. This effect was dose related and was most evident when given in regimens including days 5-7 or days 9-10 or pregnancy. LRF also has antigonadal effects, but at much higher doses than A. The use of corn oil vs. 0.1% gelatin-saline improved the effectiveness of low doses of A. Termination of pregnancy in A- or LRF-treated rats is most probably due to the markedly diminished progesterone secretion, which could result from the secretion of biologically inactive gonadotropins, reduced pituitary responsiveness to endogenous LRF, or down-regulation of gonadal receptors for LH.
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The opiate-like peptide beta-endorphin and adrenocorticotropin are concomitantly secreted in increased amounts by the adenohypophysis in response to acute stress or long-term adrenalectomy as well as in vitro in response to purified corticotropin releasing factor and other secretagogues. Conversely, administration of the synthetic glucocorticoid dexamethasone inhibits the secretion of both adrenocorticotropin and beta-endorphin. Thus, both hormones possess common and identical regulatory mechanisms and there may be a functional role for circulating beta-endorphin.
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Morphine sulfate (MS) and the opioid peptide beta-endorphin beta-LPH-(61-91) stimulate prolactin and growth hormone release in steroid-primed and non-treated male rats when injected intravenously or intracisternally. On a molar basis beta-endorphin is at least 20 times more potent than MS, whereas Met5-enkephalin (beta-LPH-(61-65)) and alpha-endorphin (beta-LPH-(61-76)) are devoid of activity at the dose injected (300 mug). The in vivo stimulatory effects of beta-endorphin on prolactin secretion are reversed by the opiate antagonist naloxone. The absence of in vitro effect of MS and beta-endorphin on prolactin and growth hormone secretion by cultured rat pituitary cells suggest that they have a central nervous system site of action.
Neurotensin (NT), substance P (SP) and morphine sulfate (MS) elevate plasma prolactin and growth hormone levels in both normal or estrogen-progesterone pretreated male rats. By contrast, steroid priming is required for TRF to exhibit PRL-releasing activity. Naloxone, an opiate receptor blocker, reverses the stimulatory effect of MS only. Diphenhydramine, a histamine antagonist, inhibits the response to NT, SP and MS without affecting the response to TRF. These results suggest the involvement of a histaminic step in the action of NT, SP and MS. TRF, NT and SP do not appear to stimulate PRL and GH through activation of an opiate receptor.
Histamine releases prolactin (PRL) in estrogen-progesterone primed male rats after both iv and intracisternal (ic) injection, but does not affect in vitro PRL secretion. This stimulatory effect is reversed by the alpha-adrenergic antagonist phenoxybenzamine and the histamine antagonist diphenhydramine, gamma-Amino butyric acid (GABA), which has little in vivo effect of its own, interferes with the activity of histamine and a variety of other stimulators of PRL secretion. These results suggest the involvement of the naturally-occurring substances histamine and GABA in the central regulation of PRL secretion.
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