Evidence for a stimulatory β-adrenergic component in the release of the ovulatory LH surge in pro-oestrous rats

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Abstract
The effect on ovulation of intraventricular infusions of noradrenaline, adrenaline and various pharmacological agents acting on the adrenergic receptor subtypes were investigated in cyclic female rats on the day of pro-oestrus. The inhibitory effects on ovulation of the different infusions were monitored by administering the drugs before 11.00 h (several hours before the critical period for the ovulatory LH surge). In experiments designed to show how the drugs under investigation might stimulate ovulation, pentobarbitone sodium (35 mg/kg) was given at 14.30 h; this anaesthetic inhibits ovulation and its effects can be overcome by substances that advance the preovulatory LH surge. Noradrenaline (an α-agonist) stimulated ovulation when administered on the morning of pro-oestrus to rats injected with pentobarbitone early in the afternoon of the same day. Phenoxybenzamine and phentolamine (non-selective α-antagonists) and clonidine (a selective α2-agonist) all inhibited ovulation when infused on the morning of pro-oestrus. Yohimbine (a moderately selective α2-antagonist) neither stimulated nor inhibited ovulation. Both isoprenaline (a non-selective β-agonist) and fenoterol (a selective β2-agonist) stimulated ovulation in pentobarbitone-treated rats when administered on the morning of pro-oestrus and fenoterol was also able to overcome the pentobarbitone block when infused later in the afternoon. Propranolol (a non-selective β-antagonist) and metoprolol (a selective β1-antagonist) were stimulatory only when administered in the afternoon. Adrenaline (both an α- and β-agonist), prenalterol (a selective β1-agonist), atenolol (a selective β1-antagonist) and ICI 118, 551 (a selective β2-antagonist) neither stimulated nor inhibited ovulation. The effect of intraventricular infusions of two selected β-adrenergic drugs was also investigated in ovariectomized rats primed with 2 μg oestradiol benzoate 48 h previously. Isoprenaline and fenoterol were able to stimulate LH release at 40 and 10 min respectively after their administration. These results suggest a possible involvement of a stimulatory β2-adrenergic component in the neural regulation of the preovulatory LH surge along with the well-documented α-stimulatory component, which together may mask the possible inhibitory effects of a β1-adrenergic system. J. Endocr. (1985) 106, 143–151