Effect of exogenous β-endorphin on anterior pituitary hormone secretion in man

1982 ◽  
Vol 99 (1) ◽  
pp. 9-13 ◽  
Author(s):  
Tsutomu Oyama ◽  
Ryuji Yamaya ◽  
Toshiro Jin ◽  
Tsuyoshi Kudo
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Human Subjects ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Adrenocortical Function ◽  
Control Group ◽  
Pituitary Hormone ◽  
Plasma Acth ◽  
Anterior Pituitary Hormone

Abstract. The effect of large amounts of synthesized human β-endorphin (β-Ep) administered intrathecally on pituitary-adrenocortical function was investigated by determining the plasma levels of ACTH, cortisol, growth hormone and prolactin in 8 patients with pain caused by severe disseminated cancer. They were divided into 2 groups, an Ep group of 8 patients and a control group of 5 of the same 8 patients. There were no significant effects of β-Ep on plasma ACTH, cortisol and growth hormone levels. However, the injection of β-Ep into human subjects resulted in a rise in plasma concentrations of prolactin.

The effect of Low-Dose Dopamine Infusion on Anterior Pituitary Hormone Secretion in Normal Female Subjects

1984 ◽  
Vol 67 (2) ◽  
pp. 219-223 ◽  
Author(s):  
J. M. C. Connell ◽  
S. G. Ball ◽  
G. C. Inglis ◽  
G. H. Beastall ◽  
D. L. Davies
Keyword(s):  
Anterior Pituitary ◽  
Low Dose ◽  
Hormone Secretion ◽  
Serum Prolactin ◽  
Control Group ◽  
Pituitary Hormone ◽  
Normal Female ◽  
Dopamine Infusion ◽  
Anterior Pituitary Hormone ◽  
Female Subjects

1. The effect of low-dose dopamine infusion on anterior pituitary hormone secretion in a group of seven healthy female subjects is reported. Subjects were infused with NaCl solution (154 mmol/l) (control) or dopamine (0.01 and 0.1 μg min−1 kg−1 for 120 min at each rate) on separate days in the early follicular phase of consecutive menstrual cycles. 2. Serum prolactin decreased during infusion of dopamine at 0.01 μg min−1 kg−1 but a similar fall was found in the control group. 3. When the rate of dopamine infusion was increased to 0.1 μg min−1 kg−1 a further substantial decrease in prolactin concentration occurred, whereas prolactin in the control group showed no change. At the end of the period of dopamine infusion at 0.1 μg min−1 kg−1 serum prolactin remained significantly (P<0.025) lower than in the control group (85 ± 12 vs 180 ± 21 m-units/l). 4. No change in thyrotrophin (TSH), growth hormone (GH) or luteinizing hormone (LH) was seen during either rate of dopamine infusion compared with control. 5. While dopamine infusion at 0.1 μg min−1 kg−1 caused significant inhibition of prolactin secretion in normal female subjects, other pituitary hormone secretion was not affected: it is suggested that under the conditions of this study dopamine in hypophysial portal blood is not of primary importance in the control of basal TSH, GH and LH release.

The differential effects of galanin-(1—30) and -(3—30) on anterior pituitary hormone secretion in vivo in humans

2000 ◽  
Vol 278 (6) ◽  
pp. E1060-E1066 ◽  
Author(s):  
Jeannie F. Todd ◽  
C. Mark B. Edwards ◽  
Mohammad A. Ghatei ◽  
Stephen R. Bloom
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Area Under The Curve ◽  
Pituitary Hormone ◽  
Receptor Subtypes ◽  
Galanin Receptor ◽  
Releasing Hormone ◽  
Anterior Pituitary Hormone

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.

Tubero-infundibular dopaminergic function in cirrhotic patients: evaluation by nomifensine and domperidone

1983 ◽  
Vol 103 (3) ◽  
pp. 315-320 ◽  
Author(s):  
G. C. Monza ◽  
M. Lampertico ◽  
S. Locatelli ◽  
L. Sali ◽  
D. Cocchi
Keyword(s):  
Growth Hormone ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Pituitary Hormone ◽  
Gh Secretion ◽  
Anterior Pituitary Hormone ◽  
Slight Elevation ◽  
Cirrhotic Patients ◽  
Normal Controls ◽  
Age And Sex

Abstract. Cirrhotic patients reportedly show alterations of anterior pituitary hormone secretion, which may reflect an underlying defective central neurotransmitter function. In this study, we have investigated the catecholaminergic control of prolactin (Prl) and growth hormone (GH) secretion in cirrhotic patients by means of an indirectly acting dopamine (DA) and norepinephrine agonist, nomifensine (Nom), and a DA receptor antagonist, domperidone (Dom). Basal GH levels were higher in the 12 female and male cirrhotic patients than in the 12 age- and sex-matched normal controls, while no difference was present in basal Prl values. Administration of Nom (200 mg po) suppressed basal Prl levels (at least 30% inhibition at three consecutive times post-drug administration) in 6/12 controls and in 6/12 cirrhotic patients, the frequency of negative responses not being different between the two groups. Nom induced a slight elevation of GH levels in controls, and evoked a more marked and sustained GH increase in cirrhotic patients. Administration of Dom (4 mg iv) induced similar Prl increments in 6 male controls and 6 male cirrhotic patients. Normal Prl responsiveness to Nom and Dom points to the existence of preserved tubero-infundibular DA function and modulation of pituitary DA receptors in the cirrhotic patients investigated. Higher GH responsiveness to Nom is compatible with a different bioavailability of the drug.

Vasopressin as a neuroendocrine regulator of anterior pituitary hormone secretion

1993 ◽  
Vol 129 (6) ◽  
pp. 489-496 ◽  
Author(s):  
Andreas Kjær
Keyword(s):  
Arginine Vasopressin ◽  
Mode Of Action ◽  
Anterior Pituitary ◽  
Hormone Secretion ◽  
Pituitary Hormones ◽  
Pituitary Hormone ◽  
Anterior Pituitary Hormones ◽  
Anterior Pituitary Hormone

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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