Effects of H1 and H2 Histamine Receptor Antagonists on Positive Feed-Back Effect of Estrogen on LH in Prepubertal Female Rats
J. A. Moguilevsky, Berta Szwarcfarb, María R. Faigón, John F. Paolini, Pablo Scacchi
Abstract
J. A. Moguilevsky, Berta Szwarcfarb, María R. Faigón, John F. Paolini, Pablo Scacchi
Abstract
The aim of the present study was to determine whether histaminergic central mechanisms which exert a well known effect on gonadotrophin secretion are involved in the development of the positive feed-back effect of estrogen-progesterone (E-P) on LH secretion that normally occurs in female rats about 20-22 days old. The administration of histamine H2 (cimetidine and ranitidine) or H1 (diphenhydramine) receptor blocking agents did not modify the onset of the LH release response to E-P. Nevertheless cimetidine, ranitidine and diphenhydramine potentiated the LH release induced by ovarian steroids at 23 days of age. These results appear to indicate that histaminergic pathways are involved in the magnitude of the LH response to E-P in prepubertal female rats rather than in the maturation of this mechanism.
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The aim of the present study was to determine whether histaminergic central mechanisms which exert a well known effect on gonadotrophin secretion are involved in the development of the positive feed-back effect of estrogen-progesterone (E-P) on LH secretion that normally occurs in female rats about 20-22 days old. The administration of histamine H2 (cimetidine and ranitidine) or H1 (diphenhydramine) receptor blocking agents did not modify the onset of the LH release response to E-P. Nevertheless cimetidine, ranitidine and diphenhydramine potentiated the LH release induced by ovarian steroids at 23 days of age. These results appear to indicate that histaminergic pathways are involved in the magnitude of the LH response to E-P in prepubertal female rats rather than in the maturation of this mechanism.
Key concepts: Histaminergic, Endocrinology, Internal medicine, Cimetidine, Histamine, Diphenhydramine, Ranitidine, Estrogen