Studies on Growth Hormone Secretion: VII. Effects of Somatostatin on Plasma GH, Insulin, and Glucagon in Sheep

Diabetes ◽  
1975 ◽  
Vol 24 (9) ◽  
pp. 842-850 ◽  
Author(s):  
D. Bryce ◽  
M. Yeh ◽  
C. Funderburk ◽  
H. Todd ◽  
F. Hertelendy
1987 ◽  
Vol 253 (4) ◽  
pp. E354-E359
Author(s):  
K. Ishikawa ◽  
H. Katakami ◽  
L. A. Frohman

The inhibitory effect of centrally administered thyrotropin-releasing hormone (TRH) on the plasma growth hormone (GH) response to GH-releasing hormone (GHRH) in the rat was studied in relation to the anatomic loci involved. Experiments were performed in animals with bilateral electrolytic lesions in the medial preoptic (MPO) area or with anterolateral hypothalamic deafferentation and in sham-operated controls. Blood samples were obtained every 10 to 20 min from and drugs were injected into freely moving animals with indwelling cannulas in the right atrium and lateral cerebral ventricle. In control animals, the plasma GH response to GHRH, 1 microgram iv, was almost completely inhibited by TRH, 1 microgram icv, injected 5 min previously. In animals with either MPO lesions or anterolateral hypothalamic deafferentation in which median eminence somatostatin immunochemical staining was almost completely eliminated, the GH response to GHRH was enhanced and TRH did not exhibit any inhibitory effect. These results, together with the previous observation that the inhibitory effect of TRH is blocked by prior treatment with anti-somatostatin serum, suggest that the effect of TRH is mediated by stimulation of somatostatin-containing neurons in the periventricular nucleus of the MPO area.


1995 ◽  
Vol 144 (1) ◽  
pp. 83-90 ◽  
Author(s):  
E Magnan ◽  
L Mazzocchi ◽  
M Cataldi ◽  
V Guillaume ◽  
A Dutour ◽  
...  

Abstract The physiological role of endogenous circulating GHreleasing hormone (GHRH) and somatostatin (SRIH) on spontaneous pulsatile and neostigmine-induced secretion of GH was investigated in adult rams actively immunized against each neuropeptide. All animals developed antibodies at concentrations sufficient for immunoneutralization of GHRH and SRIH levels in hypophysial portal blood. In the anti GHRH group, plasma GH levels were very low; the amplitude of GH pulses was strikingly reduced, although their number was unchanged. No stimulation of GH release was observed after neostigmine administration. The reduction of GH secretion was associated with a decreased body weight and a significant reduction in plasma IGF-I concentration. In the antiSRIH group, no changes in basal and pulsatile GH secretion or the GH response to neostigmine were observed as compared to controls. Body weight was not significantly altered and plasma IGF-I levels were reduced in these animals. These results suggest that in sheep, circulating SRIH (in the systemic and hypophysial portal vasculature) does not play a significant role in pulsatile and neostigmine-induced secretion of GH. The mechanisms of its influence on body weight and production of IGF-I remain to be determined. Journal of Endocrinology (1995) 144, 83–90


Author(s):  
R. Collu ◽  
G. Charpenet ◽  
M. J. Clermont

SUMMARY:The intraperitoneal (IP) or intraventricular (IVT) administration of small amounts of taurine did not modify pentobarbital-induced sleep or pituitary hormone release. However, the drastic increment in plasma GH values induced by morphine administration was completely blocked by the IVT injection of the amino acid. Whether taurine plays a physiological role in the control ofGH secretion is highly speculative.


1986 ◽  
Vol 111 (1) ◽  
pp. 91-97 ◽  
Author(s):  
S. Harvey ◽  
S.-K. Lam ◽  
T. R. Hall

ABSTRACT Passive immunization of immature chickens with sheep somatostatin (SRIF) antiserum promptly increased the basal plasma GH concentration and augmented TRH-induced GH secretion. Although exogenous SRIF had no inhibitory effect on the basal GH concentration in untreated birds or birds pretreated with non-immune sheep serum, it suppressed the stimulatory effect of SRIF immunoneutralization on GH secretion. These results suggest that SRIF is physiologically involved in the control of GH secretion in birds, in which it appears to inhibit GH release tonically. J. Endocr. (1986) 111, 91–97


1991 ◽  
Vol 125 (5) ◽  
pp. 518-525 ◽  
Author(s):  
Anna-Lena Hulting ◽  
Björn Meister ◽  
Lena Carlsson ◽  
Agneta Hilding ◽  
Olle Isaksson

Abstract. The effects of the peptide galanin on growth hormone secretion were studied in vitro using cultured rat and human anterior pituitary cells, and in vivo by iv administration of galanin in both rats and humans. Galanin in concentrations from 10 nmol/l to 1 μmol/l did not alter basal GH release, but slightly inhibited GHRH-stimulated GH release from cultured rat anterior pituitary cells. Galanin (1 μmol/l) did not significantly change basal or GHRH-stimulated GH secretion from cultured human anterior pituitary cells. In contrast, iv injection of 1 μg (300 pmol) galanin to rats induced an increase in plasma GH that was reproducible at repetitive injections. The galanin-induced GH release in rats was of a lower magnitude than the increase in plasma GH after iv injections of GHRH, and was seen with a 5-15 min delay in comparison to iv administered GHRH. In man, iv infusions of galanin (40 pmol ·kg−1 · min−1 · (40 min)) also caused a significant increase in plasma GH, but it occurred 25-30 min after the beginning of the infusion. These results suggest an indirect action of galanin on GH release in both rats and humans, i.e. galanin does not directly affect the somatotropes. In agreement with a central action, no binding sites for galanin could be demonstrated in the rat anterior pituitary by autoradiography. Since galanin did not affect somatostatin release from fragments of rat mediobasal hypothalamus, the stimulatory effects of galanin on GH release are most likely mediated via a stimulatory effect on GHRH neurons.


1978 ◽  
Vol 88 (4) ◽  
pp. 676-690 ◽  
Author(s):  
Staffan Edén ◽  
Kerstin Albertsson-Wikland ◽  
Olle Isaksson

ABSTRACT Radioimmunoassayable growth hormone (GH) was determined in fed and fasted female rats of different ages. In 6–40 day-old rats blood was collected at hourly intervals in groups of rats at different time intervals during the day. Within each age group the variation in plasma GH was considerable. In 6–14 day-old rats plasma GH was generally elevated. By day 18 levels declined, lowest on day 22 and by day 26 again increasing. In 14 day-old rats the median plasma level of GH was 22 ng/ml, in 22 day-old rats < 5 ng/ml and in 40 day-old rats 43 ng/ml. In 14 day-old rats levels ranged from < 5 ng/ml – 148 ng/ml, in 22 day-old rats from < 5 ng/ml – 34 ng/ml and in 40 day-old rats from < 5 ng/ml – > 200 ng/ml. A 20 h fasting period was associated with a significant decrease in plasma GH. In 45 day-old rats, the variations in plasma GH of individual animals were studied by obtaining sequential blood samples from unrestrained, undisturbed animals with implanted intra-aortic cannulae. In these rats GH secretion was characterized by an episodic release, occurring every 2–4 h. After a 20 h fasting period major peaks were depressed and occurred less frequently. It is concluded that there is an age-related as well as a circadian rhythm in growth hormone secretion in the rat and that sequential sampling of blood is essential for the evaluation of the secretory pattern.


1986 ◽  
Vol 108 (3) ◽  
pp. 413-416 ◽  
Author(s):  
C. G. Scanes ◽  
S. Harvey ◽  
J. Rivier ◽  
W. Vale

ABSTRACT Rat hypothalamic GH-releasing factor (rhGRF), at doses between 0·1 and 10 μg/kg, increased plasma GH concentrations in immature domestic fowl 5–10 min after i.v. injection. Sodium pentobarbitone anaesthesia blunted the GH responses to rhGRF, although in both conscious and anaesthetized chicks the maximal responses were induced by a dose of 1 μg rhGRF/kg. The stimulatory effect of rhGRF on in-vivo GH secretion was less than that provoked by corresponding doses of human pancreatic GRF, but greater than that elicited by two rhGRF analogues, (Nle27)-rhGRF(1–32) and (Nle27)-rhGRF(1–29). These results demonstrate that the chicken pituitary is responsive to mammalian GRF and provide evidence of structure-activity relationships of GRF in the domestic fowl. J. Endocr. (1986) 108, 413–416


1972 ◽  
Vol 54 (2) ◽  
pp. 195-206 ◽  
Author(s):  
F. MASSARA ◽  
F. CAMANNI

SUMMARY The effects of various adrenergic substances, either alone or in association with alpha and beta blocking agents, on human plasma growth hormone (GH) were studied in 36 normal volunteers. Plasma GH levels were unaffected by i.v. adrenaline (10 μg/min for 30 min) or by propranolol (1·5 mg/min for 10 min). Given together at the same doses, these drugs provoked sharp increases in plasma GH (from 8·5 to > 100 ng/ml; a mean increase of 30±8·02 (s.e.m.)). Reduction of the adrenaline dose to 7 μg/min produced a positive response in four out of six cases. The GH response to propranolol plus adrenaline was suppressed by simultaneous administration of phentolamine, but not significantly altered by glucose and aminophylline. Noradrenaline (7–14 μg/min for 30 min) produced no changes in plasma GH levels in six cases, while its association with propranolol was followed by an increase in only one out of four cases. Phenylephrine and tyramine were without effect, with or without propranolol. In five out of six cases, GH values gradually increased after oral administration of 1 g l-DOPA (from 4·2 to 85 ng/ml; mean, 30·2). This response was totally suppressed by phentolamine. It is considered that stimulation of GH by propranolol plus adrenaline and l-DOPA is mediated by alpha-adrenergic receptors. The possible role of a beta-inhibiting effect is discussed.


1979 ◽  
Vol 91 (3) ◽  
pp. 428-436 ◽  
Author(s):  
Ichiji Wakabayashi ◽  
Megumi Kanda ◽  
Nobuyasu Miki ◽  
Reiko Demura ◽  
Kazuo Shizume

ABSTRACT Effects of chlorpromazine (CPZ) on plasma GH and prolactin levels were observed in conscious rats provided with chronic indwelling right atrial cannulae. The administration of CPZ (200 μg/100 g b.w. iv) suppressed episodic plasma GH burst and resulted in significant elevations of plasma prolactin levels. These were also observed in rats in which two types of hypothalamic deafferentation, i.e. anterior and complete, had been carried out. The data suggest that CPZ acts within the medial basal hypothalamus and inhibits episodic plasma GH secretion. In addition, it is inferred that catecholamines are involved in the generation of episodic plasma GH burst.


1990 ◽  
Vol 126 (2) ◽  
pp. 237-244 ◽  
Author(s):  
R. W. Lea ◽  
C. A. Ahene ◽  
J. A. Marsh ◽  
S. Harvey

ABSTRACT The i.c.v. administration of 0·1 or 10 μg ovine (o)GH to 12- to 16-week-old hypothyroid chickens of a sex-linked dwarf (SLD) strain suppressed the basal plasma GH concentrations, measured 24 h afterwards. The GH response of the oGH-injected SLDs to TRH was suppressed, in a dose-related way, in comparison with that induced by TRH in birds given control injections (10 μg) of bovine serum albumin (BSA). Basal circulating concentrations of GH in euthyroid K strain birds of the same age were even lower than in the SLDs following injection of 10 μg oGH, and were not further reduced by oGH administration. The GH response to TRH in the K strain birds injected i.c.v. with 0·1 or 10 μg oGH was, nevertheless, suppressed in comparison with the BSA-injected K strain controls. The i.c.v. administration of oGH also suppressed circulating concentrations of LH and the LH response to TRH in the K strain birds. Twenty-four hours after i.c.v. administration of oGH (10 μg), the somatostatin (SRIF) content in the medial basal hypothalamus of 8-week-old euthyroid cockerels was greater than that in BSA (10 μg)-injected controls. At the same time, the binding of [3H]3-methyl-histidine2-TRH to the pituitary caudal and cephalic lobes of GH-injected birds was less than that in the controls. These results suggest that GH regulation in avian species is partly mediated by an inhibitory short-loop mechanism (mediated by hypothalamic SRIF and a down-regulation of pituitary TRH-binding sites) that suppresses basal and secretagogue-induced GH release. Journal of Endocrinology (1990) 126, 237–244


Sign in / Sign up

Export Citation Format

Share Document