Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion

1993 ◽  
Vol 129 (6) ◽  
pp. 489-496 ◽  
Author(s):  
Andreas Kjær

Secretion of the anterior pituitary hormones adrenocorticotropin (ACTH), β-endorphin and prolactin (PRL) is complex and involves a variety of factors. This review focuses on the involvement of arginine-vasopressin (AVP) in neuroendocrine regulation of these anterior pituitary hormones with special reference to receptor involvement, mode of action and origin of AVP. Arginine-vasopressin may act via at least two types of receptors: V1− and V2−receptors, where the pituitary V1−receptor is designated V1b. The mode of action of AVP may be mediating, i.e. anterior pituitary hormone secretion is transmitted via release of AVP, or the mode of action may be permissive, i.e. the presence of AVP at a low and constant level is required for anterior pituitary hormones to be stimulated. Under in vivo conditions, the AVP-induced release of ACTH and β-endorphin is mainly mediated via activation of hypothalamic V1− receptors, which subsequently leads to the release of corticotropin-releasing hormone. Under in vitro conditions, the AVP-stimulated release of ACTH and β-endorphin is mediated via pituitary V1b− receptors. The mode of action of AVP in the ACTH and β-endorphin response to stress and to histamine, which is involved in stress-induced secretion of anterior pituitary hormones, is mediating (utilizing V1− receptors) as well as permissive (utilizing mainly V1− but also V2−receptors). The AVP-induced release of PRL under in vivo conditions is conveyed mainly via activation of V1−receptors but V2−receptors and probably additional receptor(s) may also play a role. In stress- and histamine induced PRL secretion the role of AVP is both mediating (utilizing V1 −receptors) and permissive (utilizing both V1− and V2− receptors). Arginine-vasopressin may be a candidate for the PRL-releasing factor recently identified in the posterior pituitary gland. Arginine-vasopressin of both magno- and parvocellular origin may be involved in the regulation of anterior pituitary hormone secretion and may reach the corticotrophs and the lactotrophs via three main routes: the peripheral circulation, the long pituitary portal vessels or the short pituitary portal vessels.

Physiology ◽  
1999 ◽  
Vol 14 (2) ◽  
pp. 54-58
Author(s):  
W. R. Crowley

The hypothalamus regulates the secretion of anterior pituitary hormones via release of releasing hormones into the hypophysial portal vasculature. Additional neuromessengers act at the pituitary to modulate responses to the hypothalamic hormones. For example, neuropeptide Y enhances the effect of gonadotropin-releasing hormone and the response to the prolactin-inhibiting hormone dopamine.


1983 ◽  
Vol 260 (1) ◽  
pp. 99-106 ◽  
Author(s):  
Ivan S. Login ◽  
Michael J. Cronin ◽  
S.W.J. Lamberts ◽  
Carlos A. Valdenergro ◽  
Robert M. MacLeod

1991 ◽  
Vol 125 (4) ◽  
pp. 378-384 ◽  
Author(s):  
William H. Meller ◽  
David A. Lewis ◽  
Timothy L. Gehris ◽  
Roger G. Kathol

Abstract. The adrenocorticotropin-releasing effect of arginine vasopressin is well known. The effects of AVP on other anterior pituitary hormones remain confusing, with few in vivo human data available. Two human studies of exogenous AVP effects on ACTH, GH, TSH and prolactin are described. In the dosage and route of administration used, AVP was found to be a specific ACTH secretagogue.


2008 ◽  
Vol 42 (2) ◽  
pp. 171-183 ◽  
Author(s):  
Laura E Ellestad ◽  
Stefanie A Malkiewicz ◽  
H David Guthrie ◽  
Glenn R Welch ◽  
Tom E Porter

The expression profile of glucocorticoid-induced leucine zipper (GILZ) in the anterior pituitary during the second half of embryonic development in the chick is consistent with in vivo regulation by circulating corticosteroids. However, nothing else has been reported about the presence of GILZ in the neuroendocrine system. We sought to characterize expression and regulation of GILZ in the chicken embryonic pituitary gland and determine the effect of GILZ overexpression on anterior pituitary hormone levels. Pituitary GILZ mRNA levels increased during embryogenesis to a maximum on the day of hatch, and decreased through the first week after hatch. GILZ expression was rapidly upregulated by corticosterone in embryonic pituitary cells. To determine whether GILZ regulates hormone gene expression in the developing anterior pituitary, we overexpressed GILZ in embryonic pituitary cells and measured mRNA for the major pituitary hormones. Exogenous GILZ increased prolactin mRNA above basal levels, but not as high as that in corticosterone-treated cells, indicating that GILZ may play a small role in lactotroph differentiation. The largest effect we observed was a twofold increase in FSH β subunit in cells transfected with GILZ but not treated with corticosterone, suggesting that GILZ may positively regulate gonadotroph development in a manner not involving glucocorticoids. In conclusion, this is the first report to characterize avian GILZ and examine its regulation in the developing neuroendocrine system. We have shown that GILZ is upregulated by glucocorticoids in the embryonic pituitary gland and may regulate expression of several pituitary hormones.


2000 ◽  
Vol 278 (6) ◽  
pp. E1060-E1066 ◽  
Author(s):  
Jeannie F. Todd ◽  
C. Mark B. Edwards ◽  
Mohammad A. Ghatei ◽  
Stephen R. Bloom

Intravenous injection of galanin increases plasma growth hormone (GH) and prolactin (PRL) concentrations. In the rat, the effects of galanin on GH appear to be mediated via the hypothalamic galanin receptor GAL-R1, at which galanin-(3—29) is inactive. In contrast, the effect of galanin on PRL is mediated via the pituitary-specific galanin receptor GAL-RW, at which galanin-(3—29) is fully active. We investigated the effects of an intravenous infusion of human galanin (hGAL)-(1—30) and -(3—30) on anterior pituitary hormone levels in healthy females. Subjects were infused with saline, hGAL-(1—30) (80 pmol ⋅ kg− 1 ⋅ min− 1), and hGAL-(3—30) (600 pmol ⋅ kg− 1 ⋅ min− 1) and with boluses of gonadotropin-releasing hormone, thyrotropin-releasing hormone, and growth hormone-releasing hormone (GHRH). Both hGAL-(1—30) and -(3—30) potentiated the rise in GHRH-stimulated GH levels [area under the curve (AUC), saline, 2,810 ± 500 vs. hGAL-(1—30), 4,660 ± 737, P < 0.01; vs. hGAL-(3—30), 6,870 ± 1,550 ng ⋅ min ⋅ ml− 1, P < 0.01]. In contrast to hGAL-(1—30), hGAL-(3—30) had no effect on basal GH levels (AUC, saline, −110 ± 88 vs. hGAL 1—30, 960 ± 280, P < 0.002; vs. hGAL-(3—30), 110 ± 54 ng ⋅ min ⋅ ml− 1, P = not significant). These data suggest that the effects of galanin on basal and stimulated GH release are mediated via different receptor subtypes and that the human equivalent of GAL-RW may exist.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Junpei Yamashita ◽  
Yuji Nishiike ◽  
Thomas Fleming ◽  
Daichi Kayo ◽  
Kataaki Okubo

AbstractThe preoptic area (POA) is one of the most evolutionarily conserved regions of the vertebrate brain and contains subsets of neuropeptide-expressing neurons. Here we found in the teleost medaka that two neuropeptides belonging to the secretin family, pituitary adenylate cyclase-activating polypeptide (Pacap) and vasoactive intestinal peptide (Vip), exhibit opposite patterns of sexually dimorphic expression in the same population of POA neurons that project to the anterior pituitary: Pacap is male-biased, whereas Vip is female-biased. Estrogen secreted by the ovary in adulthood was found to attenuate Pacap expression and, conversely, stimulate Vip expression in the female POA, thereby establishing and maintaining their opposite sexual dimorphism. Pituitary organ culture experiments demonstrated that both Pacap and Vip can markedly alter the expression of various anterior pituitary hormones. Collectively, these findings show that males and females use alternative preoptic neuropeptides to regulate anterior pituitary hormones as a result of their different estrogen milieu.


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