Ovarian function is well known to be regulated by hypothalamic-pituitary-ovarian hormones. While several histological studies have described the autonomic innervation of the ovary, the roles of these autonomic nerves in ovarian function were unclear. Our previous study showed that ovarian estradiol secretion is controlled by sympathetic adrenergic innervation. Of the two pathways of sympathetic nerves to the ovary (superior ovarian nerve: SON and ovarian nerve plexus: ONP), stimulation of the SON, but not of the ONP, reduces estradiol secretion through the activation of alpha 2-adrenoceptors but not of alpha 1-adrenoceptors. Estradiol is synthetized from testosterone by aromatization in the ovary. In this study, we examined whether the inhibitory effect of SON on estradiol secretion via activation of alpha 2-adrenoceptors is a secondary response to an inhibitory effect of sympathetic nerve stimulation on testosterone.
The rats were anesthetized on the day of estrous, and the ovarian venous blood was collected intermittently from the ovarian vein. The secretion rate of testosterone from the ovary was calculated from the difference in the testosterone concentration between ovarian venous plasma and systemic arterial blood plasma, and the rate of ovarian venous plasma flow. The distal part of the severed SON was electrically stimulated at a supramaximal intensity for C-fibers for 5 min. Under resting condition, mean basal level of testosterone secretion rate was 26.8 + 6.3 pg/min. Secretion rate of testosterone was significantly decreased by 26.4 + 5.6% during the SON stimulation. The reduction of the testosterone secretion rate by SON stimulation was not influenced by an alpha 2-adrenoceptor antagonist (yohimbine), but it was abolished by an alpha 1-adrenoceptor antagonist (prazosin).
These results show that SON has an inhibitory role in ovarian testosterone secretion, via activation of alpha 1-adrenoceptors, but not alpha 2-adrenoceptors. Since inhibition of ovarian estradiol secretion by SON stimulation mediates alpha 2-adrenoceptors but not alpha 1-adrenoceptors, it is concluded that the reduction of estradiol secretion by SON stimulation is due to direct inhibition of estradiol production.