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Rats with a 4-day oestrous cycle were injected with 2·5 mg haloperidol/kg, a dopaminergic blocker, or with 2·0 mg propranolol/kg, a β₁- and β₂-receptor blocker, at 13.00 h on oestrus, dioestrous day 1, diestrous day 2 or pro-oestrus. Animals were autopsied on the next expected day of oestrus. Haloperidol blocked ovulation when injected on oestrus, dioestrous day 1 or pro-oestrus and was less effective when injected on dioestrous day 2. Propranolol caused a decrease in the number of ova shed when injected on dioestrous day 2 or pro-oestrus. Serum concentrations of FSH at oestrus were below the control values in those animals in which ovulation was blocked by haloperidol. No significant changes in serum concentrations of LH were observed. The normal gonadotrophin peak which occurs during the afternoon of pro-oestrus was blocked by administration of haloperidol on oestrus or dioestrous day 1. Administration of gonadotrophin-releasing hormone (GnRH) to haloperidol-treated animals on oestrus or dioestrous day 1 did not restore ovulation or increase serum FSH levels. When the same dose of GnRH was given to rats treated with haloperidol on pro-oestrus, they all ovulated and their FSH levels rose normally. Treatment with both FSH and LH of rats given haloperidol at oestrus restored ovulation in 50% of the animals, whereas it was ineffective in animals treated on dioestrous day 1. Fifty per cent of the animals treated with haloperidol on oestrus or dioestrous day 1 ovulated when oestradiol benzoate was injected on dioestrous day 2.

These results suggest that the dopaminergic and adrenergic systems have different roles in the regulation of the oestrous cycle and ovulation. The decrease in the number of ova shed induced by propranolol may be related to the blockade of receptors at the level of the ovary. The sensitivity of the dopaminergic systems involved in gonadotrophin control seems to vary depending on the day of the oestrous cycle. It is possible that when the dopaminergic system is blocked at the beginning of the cycle, an alteration in oestrogen secretion might be produced, initiating a chain of events at the hypothalamic-pituitary-ovarian axis which will ultimately inhibit ovulation. Since dopaminergic blockade induces an increase in prolactin secretion, and prolactin enhances dopamine turnover at the median eminence and blocks oestrogen secretion at the level of the ovary, the present results might also reflect the effects of haloperidol at two different levels, i.e. increased dopamine turnover at the median eminence and decreased secretion of oestrogens.

J. Endocr. (1987) 113, 37–44