Adrenergic intracerebroventricular stimulation affects progesterone concentration in the ovarian vein of the rat: participation of the superior ovarian nerve

Abstract

The present study investigates the acute consequences of central adrenergic stimulation on the release of steroids from the ovary. The influence of the superior ovarian nerve (SON) and the relationship between the neural effect and peripheral LH levels were also examined.The intracerebroventricular (i.c.v.) injection of 5 µg epinephrine in SON-intact rats on day 1 of dioestrus (D1) increased progesterone levels in ovarian vein blood from 7 to 21 min after injection but the same injection in SON-intact rats on day 2 of dioestrus (D2) decreased progesterone levels in ovarian vein blood from 1 to 25 min. A smaller dose (0·5 µg) of epinephrine injected i.c.v. in SON-intact rats produced a decrease in progesterone levels in ovarian vein blood of shorter duration. In SON-transected (SONt) animals, 0·5 µg epinephrine i.c.v. caused a smaller decrease in progesterone levels compared with SON-intact rats (P<0·05). On the other hand, in SON-intact rats on D2, the i.c.v. injection of 0·5 µg epinephrine did not modify the peripheral LH levels during 25 min, but 5 µg epinephrine injected i.c.v. raised the peripheral LH level from the third minute after injection (P<0·05). Oestradiol levels in the ovarian vein blood did not change after epinephrine i.c.v. injection in rats on D2.To avoid any humoral influence, SONt and SONintact rats on D2 were injected i.c.v. with 5 µg epinephrine or with vehicle, and 5 min later the ovaries were incubated in vitro with or without LH. Under these conditions, it was demonstrated that the previous injection of epinephrine in SON-intact rats resulted in a diminished release of progesterone from ovaries incubated with or without LH.These results suggest that a central adrenergic stimulus increases progesterone release from the ovary on D1 and decreases it on D2. Also, this neural input would arrive at the ovary through the SON, and would condition the ovarian response to LH on D2. Ovarian progesterone changes could be attributed to signals coming from ganglionar neurons, which are affected by the central adrenergic stimulation.

The cholinergic influence on the mesenteric ganglion affects the liberation of ovarian steroids and nitric oxide in oestrus day rats: characterization of an ex vivo system

“…Experiments carried out in our laboratory have shown that coeliac ganglion stimulus with cholinergic agents and an adrenergic agent modifies the ovarian steroids release through the superior ovarian nerve (Sosa et al 2000, Casais et al 2001. On the other hand, the intracerebroventricular injection of epinephrine modifies rapidly the concentration of progesterone in the ovarian vein of dioestrus day 1 and dioestrus day 2 rats (De Bortoli et al 1998). This may provide physiological evidence of the participation, at least in part, of the sympathetic ganglionic pathway in the responses observed, acetylcholine being the classic preganglionic neurotransmitter.…”

Involvement of the coeliac ganglion in the luteotrophic effect of androstenedione in late pregnant rats

“…The stimulation of lipolysis and the increased blood flow through the ovary could supply the corpus luteum with serum-derived lipoproteins as a source of cholesterol for luteal steroidogenesis (Williams 1989). In studies in conscious heifers, the infusion of NA into the abdominalis aorta stimulated the secretion of progesterone within a few minutes in a dose-dependent manner (Kotwica et al 2002). De Bortoli et al (1998 demonstrated that a central adrenergic stimulus produces acute effects on the release of steroids from the ovary.…”

Release of ovarian progesterone during the rat oestrous cycle by ganglionic cholinergic influence

“…This may provide physiological evidence of the participation, at least in part, of the sympathetic ganglionic pathway, whose preganglionic neurotransmitter per excellence is acetylcholine. The superior ovarian nerve (SON) might be the neural way of the central adrenergic stimulation [7].…”