Norepinephrine modulates the effect of neuropeptides in coeliac ganglion on ovarian hormones release: its relationship with ovarian nitric oxide and nerve growth factor.

OBJECTIVE: Ovarian steroids are modulated by neural influences. In this work we investigate whether norepinephrine (NE) modifies the vasoactive intestinal peptide (VIP) or neuropeptide Y (NPY) actions in coeliac ganglion (CG) on the ovarian hormone release, and evaluate the participation of nitric oxide (NO), measured as nitrite, and of inducible nitric oxide synthetase (iNOS) protein, nerve growth factor (NGF) and its trkA receptor gene expression in the ovarian response. METHODS: The study was performed in the ex vivo CG-superior ovarian nerve (SON)-ovary system of rats on diestrus day 2 (D2). CG and ovary were placed in separate compartments connected by the SON and incubated with Krebs-Ringer buffer. After addition of 50 ng/ml VIP, 50 ng/ml NPY, 10-6 M NE, or a mix of VIP+NE or NPY+NE in ganglion, samples from the ovarian compartment were taken at different times throughout 180 minutes to measure progesterone, androstenedione and nitrite levels. RESULTS: VIP and NPY in ganglion induced an increase of progesterone release that was associated for VIP, but not NPY, with a decrease of ovarian nitrite levels, iNOS protein, and NGF/trkA receptor mRNA expression. By contrast, NE in ganglion decreased progesterone, an effect that was suppressed by addition of propranolol in ganglion, and increased nitrites/iNOS and NGF/trkA receptor expression in ovary. GABA A receptor antagonist bicuculline (20 muM) added in ovarian compartment prevented the inhibitory effect on progesterone caused by NE in CG. Androstenedione was not modified under neuropeptides or NE ganglionic stimulation. CONCLUSIONS: Finally, results from VIP+NE or NPY+NE in ganglion showed that ovarian response on D2 induced by VIP or NPY alone is moderated by the opposite action of NE, and occurs only on progesterone, the most sensitive steroid to neural action.

In vitro effect of neuropeptides on ovary or celiac ganglion affects the release of progesterone from ovaries in the rat.

BACKGROUND: The purpose of this work was to examine the in vitro effects of three neuropeptides--vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), and substance P (SP)--on the release of ovarian progesterone (Po), acting directly on the ovary (O) or on the celiac ganglion (CG) of rats in diestrus 1 (D1) and 2 (D2), because in these two cycle stages neural effects have been observed on P release. MATERIAL/METHODS: Hemiovaries of rats in D1 and D2 were incubated with each neuropeptide alone and in combination with norepinephrine. Also, the CG-superior ovarian nerve (SON)-O system was incubated with the addition of each neuropeptide to the CG. RESULTS: In D1 ovaries, NPY, VIP or SP, both alone and with norepinephrine, generally decreased the release of Po. The effect of each neuropeptide was modified by norepinephrine. In D2, NPY, VIP or SP, both alone and with norepinephrine, increased Po release. The effect of NPY and SP was modified by norepinephrine. In the CG-SON-O system, in D1, the addition of NPY and VIP alone increased Po release, while SP decreased it. In D2, the three neuropeptides increased Po release. CONCLUSIONS: Of the studied situations, only the effects of NPY and VIP on the CG during D1 mirror the changes of progesterone in blood during the rat estrous cycle. These effects are in agreement with others obtained by intracerebroventricular injection of epinephrine, suggesting that these neuropeptides might be released on CG after this injection and produce increased progesterone in blood.

Involvement of beta-adrenoceptors in a central regulation of the ovarian progesterone release in rats.

UNLABELLED: The intracerebroventricular (i.c.v.) injection of epinephrine modifies ovarian progesterone (P) release in rats on diestrus day 2 (D2). OBJECTIVES: To investigate the characteristic of a central adrenergic effect on the ovarian P release on D2. Also, the function of the superior ovarian nerve (SON) is re-examined. METHODS AND RESULTS: P concentrations were measured using radioimmunoassay techniques. The i.c.v. injection of 5 mg isoproterenol (beta-adrenergic agonist) in SON-intact rats on D2, decreased the P levels in ovarian vein blood from 1 to 25 min after injection (p<0.05). Similar treatment in SON-transected rats did not modify the P concentrations in ovarian vein blood between 1 and 25 min after injection. After 5 microg propranolol (beta-adrenergic antagonist) i.c.v. injection in SON-intact rats, the P levels in ovarian vein blood increased from 2 to 4 min (p<0.05). Similar treatment in SON-transected rats did not change the P concentrations in ovarian vein blood during 25 min after injection. The i.c.v. injection of 5 microg phenylephrine (alpha-adrenergic agonist) in SON-intact or SON-transected rats, did not modify the P levels in ovarian vein blood between 1 and 25 min after injection. After 5 microg phentolamine (alpha-adrenergic antagonist) i.c.v. injection in SON-intact or SON-transected rats, the P concentrations in ovarian vein blood did not change during 25 min. CONCLUSIONS: These results suggest the participation of central beta-adrenergic receptors in the neural regulation of the ovarian P release in rats on D2, and, furthermore, that the central beta-adrenergic input is conduced almost entirely through the superior ovarian nerve.