In-vitro control of growth hormone secretion by synthetic releasing factors in young and adult ducks (Anas platyrhynchos)

Abstract

Release of GH from perifused duckling hemipituitaries was stimulated, in a biphasic manner, by synthetic TRH and human pancreatic GH-releasing factor (GRF). At all effective concentrations, the level of GH release was increased within 5 min of TRH or GRF perifusion and was maximal after 10 min of TRH perifusion and after 20 min of GRF perifusion. Although TRH was perifused for 20 min the level of GH release declined during the last 10 min. The most effective dose of TRH (1.0 micrograms/ml; 2.7 mumol/l) and GRF (0.5 micrograms/ml; 110 nmol/l) provoked similar (250-300%) increases in the level of GH release. However, since the effect of TRH was only of short duration, the total release of GH induced by GRF was higher than that elicited by TRH, especially with the low dose. The increase in release of GH induced by TRH or GRF was blunted when pituitaries from adult ducks were used. As in young ducks, the GH response to GRF was higher, whereas the response to TRH was very low. The GH response of perifused adult pituitaries to GRF was, however, potentiated when TRH was perifused simultaneously. The basal release of GH from both young and adult pituitary glands was unaffected by perifusion with somatostatin-14 (SRIF-14) at doses of 1 and 2 micrograms/ml. The perifusion of hemipituitary glands with similar doses of SRIF-14 was also unable to suppress the stimulation of GH release induced by prior perifusion with GRF, although when SRIF-14 and TRH were simultaneously perifused TRH-induced GH release was markedly suppressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential Ontogenetic Patterns of in vitro Desensitization to GHRH in Fetal and Neonatal Anterior Pituitary

“…This desensitization could be explained by a GHRH receptor-mediated process or by the depletion of rapidly releasable GH pool, or both. These two phenomena have been reported in rats [9,10,38,39], ducks [11] and humans [40]. …”

“…This is in agreement with the data from Parenti et al [51], who showed in vivo that pretreatment with GHRH markedly reduced the effect of acute GHRH stimulation on GH release from cultured pituitary cells of young rats, but left it unchanged in old rats. In contrast, most previous reports had shown that the capacity of the pituitary gland to attenuate GH secretion in response to GHRH is developmentally regulated in the opposite way [9,10,11,12]: a higher susceptibility to homologous desensitization appeared in the most advanced stages of development (adult vs. neonatal animal or ageing vs. young animals). However, differences in the experimental model would be of relevance as they used a continuous treatment with GHRH [9,11,12], or prolonged exposure to secretagogue followed by an acute GHRH treatment [10], whereas we have used a perfusion system, allowing rapid and dynamic short-term GHRH changes.…”

“…In contrast, most previous reports had shown that the capacity of the pituitary gland to attenuate GH secretion in response to GHRH is developmentally regulated in the opposite way [9,10,11,12]: a higher susceptibility to homologous desensitization appeared in the most advanced stages of development (adult vs. neonatal animal or ageing vs. young animals). However, differences in the experimental model would be of relevance as they used a continuous treatment with GHRH [9,11,12], or prolonged exposure to secretagogue followed by an acute GHRH treatment [10], whereas we have used a perfusion system, allowing rapid and dynamic short-term GHRH changes. Our system could better represent the in vivo setting than those involving a long-term exposure to the secretagogue since the pulsatile pattern of GHRH release into the hypophyseal-portal circulation has been extensively reported [14,19,52,53].…”

“…However, our previous results in vitro [6] showed that neither basal GH release nor GHRH-induced GH release was significantly different from basal GH release or GHRH-induced GH release in fetal and neonatal pigs, suggesting that the porcine fetal somatotrope itself did not seem to be in a hyperactive state or to be hyperresponsive to GHRH. Furthermore, most of previous reports had shown that GH secretion is attenuated with aging [9,10,11,12]. This raises the important question of whether this process of attenuation in GH secretion is also present at early ages (neonates vs. fetuses); i.e.…”

The influence of thyrotropin-releasing hormone (TRH) on growth rate and thyroid activity in broiler chicks

“…In females, TRH had no effect on growth parameters. Previous observations on chickens (Harvey et al, 1978;Burkę, 1983;Leung et al, 1984;Lauterio and Scanes, 1987) and ducks (Folzer-Joudaione et al, 1988) established that TRH not only stimulates the release of thyroid hormones but also is a potent stimulant of GH secretion. Remarkable differences in GH response between małe and female broilers were seen in the form of higher plasma GH concentrations in males (Harvey et al, 1977;Johnson et al, 1990).…”