A benzodiazepine, chlordiazepoxide, blocks vasopressin and oxytocin release after footshocks but not osmotic stimulus in the rat.
Noxious as well as hypertonic stimuli potentiate vasopressin and oxytocin secretion in rats. Neurohypophysial vasopressin- and oxytocin-secreting neurons receive inhibitory synaptic inputs mediated by gamma-aminobutyric acid (GABA). Benzodiazepines modulate GABA-A receptor activity in a facilitatory fashion. It is thus possible that benzodiazepines suppress vasopressin and oxytocin release after noxious stimuli. To test this hypothesis, we investigated whether chlordiazepoxide impairs the enhanced release of vasopressin and oxytocin after noxious or hypertonic stimuli in male rats. Chlordiazepoxide (5-20 mg/kg, i.p.) blocked dose-dependently the vasopressin and oxytocin responses to footshocks. Chlordiazepoxide, however, did not impair the hormonal responses to hypertonic stimulus. The results demonstrate that chlordiazepoxide selectively prevents vasopressin and oxytocin release after noxious stimuli and therefore suggest that the sites of chlordiazepoxide actions are not on the vasopressin or oxytocin neurons in rats.
Yagi
K
K
Department of Physiology, Jichi Medical School, Tochigi-ken, Japan.
Onaka
T
T
D000818:Animals; D002707:Chlordiazepoxide / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D004597:Electroshock; D008297:Male; D009995:Osmosis; D010121:Oxytocin / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D014667:Vasopressins / Q000378:metabolism*
D014667:Vasopressins; D010121:Oxytocin; D002707:Chlordiazepoxide