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Serotonergic mechanisms involved in calcitonin potentiation of kappa-opioid receptor-mediated effects on adrenal secretion.

Abstract：

:Calcitonin can selectively modulate the effects of opioids on the rat hypothalamic-pituitary-adrenal axis and increase the release of corticosterone induced by a kappa-opioid receptor agonist. Considerable evidence supports the involvement of opioid and serotonergic systems in the analgesic effect of calcitonin. In this study, the involvement of hypothalamic serotonergic pathways in the calcitonin potentiation of the effect of (trans-(+/-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl) cyclohexyl]-benzeneacetamide methane sulphonate (U-50,488H) on the secretion of corticosterone was examined. The correlation between the calcitonin-induced potentiation of the pituitary adrenal response to U-50,488H and changes in serotonin turnover was evaluated. Our results show that the increase in the release of corticosterone induced by treatment with calcitonin + U-50,488H was not evident when the turnover of serotonin was decreased by inhibition of its synthesis with m-hydroxybenzylhydrazine (NSD 1015) or by blockade of its metabolism with trans-2-phenylcyclopropylamine (tranylcypromine). Although other factors can not be discarded, from the present data it can be suggested that the serotonergic system plays an important role in the interaction calcitonin-kappa-opioid receptor agonist in the hypothalamic-pituitary-adrenal axis.

journal_name

Eur J Pharmacol

journal_title

European journal of pharmacology

authors

Ormazábal MJ,Milanés MV,Martín MI

doi

10.1016/s0014-2999(97)01355-1

subject

Has Abstract

pub_date

1997-12-04 00:00:00

pages

81-7

issue

1

eissn

0014-2999

issn

1879-0712

pii

S0014-2999(97)01355-1

journal_volume

340

pub_type

杂志文章

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