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.
Xiao
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E
Department of Obstetrics and Gynecology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.
Xia-Zhang
L
L
Thornell
D
D
Shalts
E
E
Ferin
M
M
D000311:Adrenal Glands / Q000502:physiology; D000818:Animals; D001127:Arginine Vasopressin / Q000378:metabolism*; D003346:Corticotropin-Releasing Hormone / Q000037:antagonists & inhibitors*; D005260:Female; D006854:Hydrocortisone / Q000378:metabolism*; D007986:Luteinizing Hormone / Q000378:metabolism*; D008253:Macaca mulatta; D009270:Naloxone / Q000494:pharmacology*; D010052:Ovariectomy; D010053:Ovary / Q000502:physiology*; D013268:Stimulation, Chemical
D001127:Arginine Vasopressin; D009270:Naloxone; D007986:Luteinizing Hormone; D003346:Corticotropin-Releasing Hormone; D006854:Hydrocortisone