Adrenergic and cholinergic involvement in basal and growth hormone-releasing hormone-stimulated growth hormone secretion in glucocorticoid-treated rats

Abstract

Glucocorticoids are known to inhibit GH secretion via somatostatin. The aim of our study was to elucidate the involvement of somatostatin in the GH-releasing action of the alpha 2 agonist clonidine and the cholinergic agent pyridostigmine in conscious, freely-moving rats chronically treated with dexamethasone. After seven days of chronic glucocorticoid treatment, animals received an i.v. injection of either saline (1 ml/kg) or clonidine (150 micrograms/kg) or pyridostigmine (100 micrograms/kg) at -15 min. Three blood samples were then drawn (-10 min, -5 min, and 0 min) to assess the GH response to either clonidine or pyridostigmine alone. After the 0 min sample, saline (1 ml/kg) or GNRH (500 ng/kg) was injected i.v. and additional blood samples were drawn from 5 to 30 min. The GH response to clonidine alone or combined with GNRH in rats treated with dexamethasone was significantly lower (p < 0.05) as compared to vehicle-treated rats. The GH response to pyridostigmine alone or combined with GNRH did not significantly differ between vehicle- and dexamethasone-treated rats. These data suggest that in the rat the mechanism of action of clonidine is mainly to stimulate endogenous GNRH secretion, while pyridostigmine appears to predominantly act by decreasing hypothalamic somatostatin.

Norepinephrine Regulation of Growth Hormone Release from Goldfish Pituitary Cells. I. Involvement of α2 Adrenoreceptor and Interactions With Dopamine and Salmon Gonadotropin‐Releasing Hormone

“…The involvement of α 2 adrenoreceptors in norepinephrine inhibition of stimulated GH release is supported by the observations that the GH‐releasing actions of GnRHs and dopamine D 1 agonists can be attenuated by clonidine in goldfish pituitary cells under static incubation ( 37). It is worth mentioning that in the same animal model norepinephrine stimulates GTH release both in vivo ( 22) and in vitro ( 23) through activation of pituitary α 1 adrenoreceptors ( 24). Since norepinephrine has been shown to stimulate GnRH release from goldfish hypothalamic slices under culture conditions ( 38), a part of the GTH response induced by NE treatment in vivo may be indirect through its central action on GnRH neurones.…”

“…In our previous studies, we have shown that norepinephrine stimulates GTH release in goldfish both in vivo ( 22) and in vitro ( 23). The GTH‐releasing action of NE can be exerted directly at the pituitary cell level via α 1 adrenoreceptors ( 24). In in‐vivo experiments, intraperitoneal injection of norepinephrine induces a dose‐dependent inhibition of serum GH levels in the goldfish.…”

Effect of atropine and pyridostigmine on growth hormone response to GH‐releasing peptide‐2 and GH‐releasing hormone in swine

“…The experiment design was as in experiment 1 except that pyridostigmine at a dose of 100 µg/kg BW was used as preinjection instead of atropine (80 µg/kg BW). A dose of 100 µg/kg BW of pyridostigmine was reported to increase GH response to GHRH in rats chronically treated with dexamethasone (Giustina et al . 1995).…”

Influência dos glicocorticóides sobre o eixo somatotrófico

“…Giustina e cols. observaram que a clonidina (agonista do receptor alfa2, estimulador de GH via GHRH) e a piridostigmina (agonista colinérgico, inibidor de SRIF) foram capazes de aumentar significativamente a resposta do GH ao GHRH em ratos tratados com dexametasona por 7 dias (35). No entanto, quando administradas isoladamente, somente a clonidina foi capaz de estimular a liberação de GH, sugerindo que a ação do GHRH está intacta nestes animais, enquanto que o tônus de SRIF encontra-se elevado e refratário à ação colinérgica.…”