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

Citation
En. Xiao et al., 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, Neuroendocrinology, 64(3), 1996, pp. 225-232
Citations number
40
Categorie Soggetti
Neurosciences,"Endocrynology & Metabolism
Journal title
ISSN journal
00283835
Volume
64
Issue
3
Year of publication
1996
Pages
225 - 232
Database
ISI
SICI code
0028-3835(1996)64:3<225:TLBNTC>2.0.ZU;2-B
Abstract
In the primate, arginine vasopressin (AVP) is known to activate the hy pothalamo-pituitary-adrenal axis and to inhibit LH secretion. In the p resent study, we investigate the role of the endogenous opioid peptide s 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 experi ment 1, the effects of 5-hour i.c.v. infusions of saline (n = 7), AVP (50 mu g/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 sign ificantly decreased by AVP (p < 0.05) and by 5 h, the mean LH expresse d as a percentage from the 3-hour baseline was also significantly redu ced (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 (10 7.3 +/- 12.1% of baseline). AVP increased cortisol secretion (p < 0.05 vs. baseline), but naloxone did not prevent the increase. In experime nt 2, the LH and cortisol responses to AVP were compared in the absenc e and presence of a CRH antagonist. The antagonist was infused intrave ntricularly at two doses: 60 and 180 mu g/h. At both doses, the inhibi tory 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 no t block the AVP-induced increase in cortisol. The results confirm prev ious evidence in the primate of a role of vasopressin in inhibiting th e hypothalamo-pituitary-gonadal axis and demonstrate a role of hypotha lamic opioid peptides in this process. They also demonstrate that, alt hough CRH is a prerequisite for AVP's action on the hypothalamo-pituit ary-gonadal axis, AVP can stimulate the adrenal axis in the primate in the presence of decreased CRH activity.