Electrical stimulation of the superior ovarian nerve of intact anaesthetized dioestrous rats for 30 min reduced ovarian progesterone levels, even when papaverine and propranolol were also given. The administration of phentolamine (an alpha receptor antagonist) before stimulation reversed this effect. The results suggest that a neural control of ovarian steroidogenesis may be either excitatory through the stimulation of beta receptors or inhibitory through the stimulation of alpha receptors.

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Ovarian tissue from immature rats treated with pregnant mare serum gonadotrophin (PMSG) or PMSG and human chorionic gonadotrophin was incubated in Medium 199. Stimulation of the formation of cyclic AMP in follicular and luteal tissue by terbutaline (10(-5) mol/l), a selective beta 2-agonist, was blocked by butoxamine (10(-5) mol/l), a selective beta 2-antagonist, whereas practolol (10(-5) mol/l), a selective beta 1-antagonist, was ineffective. Propranolol (10(-5) mol/l) a non-selective beta-antagonist, butoxamine nor practolol affected the increase in cyclic AMP promoted by the addition of 1 microgram LH. Stimulation of the production of progesterone in both follicular and luteal tissue by terbutaline was blocked by butoxamine, but not by practolol. These findings indicated that beta-adrenergic stimulation of ovarian cyclic AMP and progesterone is mediated by beta 2-adrenergic receptors.

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