Neural control of somatotropic function.

Müller, E. E.

doi:10.1152/physrev.1987.67.3.962

Cited by 250 publications

(128 citation statements)

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“…In addition, xylazine has been reported to increase glucagon release from the pancreas in sheep [8]. It is well known that SRIF inhibits glucagon release from the pancreas [28]. In the present study, SRIF completely inhibited xylazine-induced hyperglycemia for the first 60 min after the xylazine injection.…”

Section: Discussionsupporting

confidence: 65%

Effects of Atipamezole, an .ALPHA.2-Adrenergic Antagonist, and Somatostatin on Xylazine-lnduced Growth Hormone Release in Calves.

et al. 1996

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Abstract. In order to clarify the mechanism of xylazine-induced GH release, we investigated the effects of atipamezole, a selective a2-adrenergic antagonist, and somatostatin (SRIF) on xylazine-stimulated GH release in calves. Xylazine injection (0.30 mg/kg BW, iv) induced a rapid increase in the GH concentration. When atipamezole was used in combination with xylazine, it blunted the increase in the plasma GH concentration induced by the xylazine injection. The GH levels at 15-50 min after the simultaneous injection of xylazine and atipamezole were significantly (P<0.05) lower than the corresponding values in the animals given xylazine alone. The area under the GH response curve for 120 min after the simultaneous injection of xylazine and atipamezole was significantly (P<0.05) smaller than that for the xylazine alone. A series of five intravenous injections of 1 mg of SRIF at 10-min intervals also blunted xylazine-stimulated GH release. Atipamezole partially suppressed xylazineinduced hyperglycemia, but SRIF completely suppressed the hyperglycemia for the first 60 min after the xylazine injection and the suppression by SRIF was stronger than that by atipamezole.On the other hand, both atipamezole and SRIF failed to blunt xylazine-induced hypoinsulinemia.The present results suggest that xylazine stimulates GH release via the a2-adrenergic pathway in cattle, but the mechanism of xylazine-induced hyperglycemia remains to be determined.

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Section: Discussionsupporting

confidence: 65%

Effects of Atipamezole, an .ALPHA.2-Adrenergic Antagonist, and Somatostatin on Xylazine-lnduced Growth Hormone Release in Calves.

et al. 1996

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“…In turn, alterations in nutritional status, such as obesity or food deprivation, markedly influence GH secretion. As GH secretion is normalized after weight loss in obesity or after refeeding in states of food deprivation, there is no doubt that altered GH secretion develops as a consequence of altered metabolic status (1)(2)(3).…”

Section: Introductionmentioning

confidence: 99%

Leptin increases in vivo GH responses to GHRH and GH-releasing peptide-6 in food-deprived rats

Carro

Seoane²,

Señarı́s³

et al. 2000

European Journal of Endocrinology

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Background: Leptin has recently been shown to have a stimulatory effect on basal GH secretion. However, the mechanisms by which leptin exert this effect are not yet clear. GHRH and GH-releasing peptide (GHRP)-6 are the two most potent GH secretagogues described to date. Objective: To determine if leptin could also enhance in vivo GH responses to a maximal dose of GHRH. Design: Leptin (10 mg i.c.v.) or vehicle was administered at random before GHRH (10 mg/kg i,v.) or GHRP-6 (50 mg/kg i.v.), to freely-moving rats with food available ad libitum and to (48 h) food-deprived rats. Methods: Leptin and GH concentrations were measured by radioimmunoassay. Comparison between the different groups was assessed by the Mann-Whitney test. Results: In comparison with fed rats, food-deprived rats showed a marked decrease in GH responses to GHRH as assessed by the area under the curve (5492 Ϯ 190 ng/ml in fed rats and 1940 Ϯ 128 ng/ml in fasted rats; P < 0.05) and GHRP-6 (3695 Ϯ 450 in fed rats and 1432 Ϯ 229 in fasted rats; P < 0.05). In comparison with its effects in vehicle-treated rats, leptin administered to food-deprived rats markedly increased GH responses to both GHRH (6625 Ϯ 613 ng/ml; P < 0.05) and GHRP-6 (5862 Ϯ 441 ng/ml; P < 0.05). Conclusions: These data suggest that the blunted GH response to GHRH and GHRP-6 in food-deprived rats is a functional and reversible state, and that the decreased leptin concentrations could be the primary defect responsible for the altered GH secretion in food-deprived rats.

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“…In addition, a complex network of neurotransmitters and hormonal, metabolic, nutritional and environmental stimuli regulate GH secretion by modulating either GHRH or SS secretion from the hypothalamus or by acting directly on the pituitary (Müller 1987).…”

Section: Introductionmentioning

confidence: 99%

Growth hormone responses to growth hormone-releasing hormone and hexarelin in fed and fasted dogs: effect of somatostatin infusion or pretreatment with pirenzepine

Rigamonti¹,

Marazzi²,

Cella³

et al. 1998

Journal of Endocrinology

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Using unanesthetized young male and female beagle dogs, before and after a 2-day fast, we studied the effect of an i.v. infusion of 0·9% saline (5 ml/h), somatostatin (SS, 4 or 8 µg/kg/h) or pretreatment with pirenzepine (PZ, 0·6 mg/kg i.v.), a muscarinic cholinergic antagonist which allegedly releases SS, on the GH release evoked by acute administration of GHRH (2 µg/kg i.v.), hexarelin (HEXA), a member of the GH-releasing peptide family (250 µg/kg i.v.) or GHRH plus HEXA.In fasted dogs, GHRH delivered during saline infusion induced a clear-cut rise in plasma GH levels, significantly higher than that which it induced in fed dogs. In contrast, HEXA, although very effective in causing the release of GH, only slightly increased GH secretion in fasted dogs over that which it induced in fed dogs. Co-administration of GHRH plus HEXA into fed dogs induced a synergic GH response that further increased with fasting.The action of GHRH in fed dogs was abolished by the lower dose of SS, whereas SS at either dose was ineffective in suppressing the GH-releasing effect during fasting. Infusion of the lower dose of SS failed to counter the action of HEXA, either before or during fasting, whilst the higher SS dose partially reduced it in both conditions.In contrast to SS, PZ reduced the GH-releasing effect of GHRH and HEXA, both in the fed state and, though to a lesser extent, during fasting. Pirenzepine only slightly reduced the robust GH rise elicited by GHRH plus HEXA in fed dogs. The suppressive effect of PZ on the GH response to combined administration of the peptides was lowest in fasted dogs.These data show that: (1) fasting augmented the GH response to GHRH and (to a lesser degree) to HEXA; (2) SS inhibited the GH response to GHRH in the fed state, but not in the fasted state; (3) only the higher dose of SS partially reduced the GH stimulation by HEXA in either the fed or the fasted state; (4) PZ lowered the GH response to GHRH and to HEXA in both the fed and (to a lesser degree) the fasted state; (5) PZ did not modify the GH release due to the combined administration of GHRH and HEXA.It is suggested that: (1) during fasting the greatly enhanced GH response to GHRH alone or GHRH plus HEXA probably reflects an augmented GHRH secretion; (2) somatotrope refractoriness to SS may contribute to the enhanced GH secretion in states of calorie deprivation; (3) in contrast to a general belief, muscarinic cholinergic antagonists, e.g. PZ, do not act exclusively via release of SS, but probably also through inhibition of GHRH function.

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Neural control of somatotropic function.

Cited by 250 publications

References 0 publications

Effects of Atipamezole, an .ALPHA.2-Adrenergic Antagonist, and Somatostatin on Xylazine-lnduced Growth Hormone Release in Calves.

Effects of Atipamezole, an .ALPHA.2-Adrenergic Antagonist, and Somatostatin on Xylazine-lnduced Growth Hormone Release in Calves.

Leptin increases in vivo GH responses to GHRH and GH-releasing peptide-6 in food-deprived rats

Growth hormone responses to growth hormone-releasing hormone and hexarelin in fed and fasted dogs: effect of somatostatin infusion or pretreatment with pirenzepine

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