Divergent Influences of the Structurally Dissimilar Calcium Entry Blockers, Diltiazem and Verapamil, on Thyrotropin- and Gonadotropin-Releasing Hormone- Stimulated Anterior Pituitary Hormone Secretion in Man*

1985 ◽  
Vol 60 (1) ◽  
pp. 144-149 ◽  
Author(s):  
JOHANNES D. VELDHUIS ◽  
JOAO L. C. BORGES ◽  
CHARLES R. DRAKE ◽  
ALAN D. ROGOL ◽  
DONALD L. KAISER ◽  
...  
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.


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.


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.


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