The luteinizing hormone but not the cortisol response to arginine vasopressin is prevented by naloxone and a corticotropin-releasing hormone antagonist in the ovariectomized rhesus monkey.

In the primate, arginine vasopressin (AVP) is known to activate the hypothalamo-pituitary-adrenal axis and to inhibit LH secretion. In the present study, we investigate the role of the endogenous opioid peptides and corticotropin-releasing hormone (CRH) in these processes. Adult ovariectomized rhesus monkeys bearing a chronic cannula in the lateral ventricle for intraventricular (i.c.v.) infusion were used. In experiment 1, the effects of 5-hour i.c.v. infusions of saline (n = 7), AVP (50 micrograms/h, n = 7), naloxone (2 mg bolus + 2 mg/h i.v., n = 4) and AVP plus naloxone (n = 4) on LH and cortisol secretion were investigated. As compared to saline and naloxone alone, LH pulse frequency was significantly decreased by AVP (p < 0.05) and by 5 h, the mean LH expressed as a percentage from the 3-hour baseline was also significantly reduced (saline 100.9 +/- 5.1%; naloxone 112.3 +/- 2.9%; AVP 63.3 +/- 8.2%). Coadministration of naloxone abolished the effects of AVP on LH (107.3 +/- 12.1% of baseline). AVP increased cortisol secretion (p < 0.05 vs. baseline), but naloxone did not prevent the increase. In experiment 2, the LH and cortisol responses to AVP were compared in the absence and presence of a CRH antagonist. The antagonist was infused intraventricularly at two doses: 60 and 180 micrograms/h. At both doses, the inhibitory effect of AVP on LH was significantly attenuated (at 4 h, 86.9 +/- 3.2% of baseline; NS vs. saline). However, the CRH antagonist did not block the AVP-induced increase in cortisol. The results confirm previous evidence in the primate of a role of vasopressin in inhibiting the hypothalamo-pituitary-gonadal axis and demonstrate a role of hypothalamic opioid peptides in this process. They also demonstrate that, although CRH is a prerequisite for AVP's action on the hypothalamo-pituitary-gonadal axis, AVP can stimulate the adrenal axis in the primate in the presence of decreased CRH activity.

Interleukin-1 stimulates luteinizing hormone release during the midfollicular phase in the rhesus monkey: a novel way in which stress may influence the menstrual cycle.

We previously demonstrated an inhibitory effect of an inflammatory/immune-like stress challenge, as simulated by intracerebroventricular interleukin-1 alpha (IL-1 alpha) administration, on LH secretion in the ovariectomized rhesus monkey. This was shown to be the result of activation of the hypothalamo-pituitary-adrenal axis by the cytokine. In the present experiments, we have investigated LH and cortisol responses to IL-1 alpha administration in intact monkeys during the follicular phase of the menstrual cycle. Eleven adult rhesus monkeys, bearing an intraventricular cannula for cytokine administration, were used. Cycle parameters were monitored in the preceding control cycles, during the experimental cycles, as well as in subsequent cycles by daily measurements of estradiol and progesterone concentrations and daily menstruation checks. The experiments were performed according to estradiol concentrations: estradiol, 5-38 pg/mL, group 1, early follicular; and estradiol, 50-64 pg/mL, group 2, midfollicular. The effects of intracerebroventricular saline (30 microL/30 min) or IL-1 alpha (4.2 micrograms/30 min) infusions on LH, FSH, and cortisol were compared. After saline infusion, there was no significant change in LH secretion. No significant acute change in LH occurred after IL-1 alpha administration in group 1 (to 0.98 +/- 0.12 ng/mL by 5 h from a baseline of 0.85 +/- 0.12); however, the length of the follicular phase was significantly prolonged in these early follicular phase animals. IL-1 significantly increased LH release in monkeys during the midfollicular phase (group 2; to 2.45 +/- 0.45 ng/mL by 5 h from a baseline of 0.88 +/- 0.11; P < 0.05 vs. baseline and all other groups). FSH was also increased in the latter group. When the experimental observation period was extended to 18 h after IL or saline treatment in eight monkeys, LH and FSH consistently increased after IL administration in three of four animals (to 4.3 +/- 0.7 ng/mL), and in one animal, a surge-like gonadotropin release occurred, whereas no further changes occurred after saline. IL-1 alpha, but not saline, significantly increased cortisol and progesterone release. In conclusion, our results demonstrate that dependent on estradiol concentrations, an acute inflammatory/immune-like stress challenge can affect the hypothalamo-pituitary-ovarian axis differently, either by stimulating gonadotropin release in the presence of significant estradiol concentrations or by inhibiting follicular maturation when given in the presence of low estradiol levels.