Compilation: Explaining Growth Inhibitions and Regulations

Norepinephrine Regulation of Growth Hormone Release from Goldfish Pituitary Cells. I. Involvement of α2 Adrenoreceptor and Interactions With Dopamine and Salmon Gonadotropin-Releasing Hormone
Authors: Lee1; Chan1; Chang2; Yunker2; Wong1
Source: Journal of Neuroendocrinology, Volume 12, Number 4, April 2000 , pp. 311-322(12)
Publisher: Blackwell Publishing

Abstract:
Adrenergic regulation of growth hormone (GH) release in the goldfish was examined in vitro using dispersed goldfish pituitary cells under column perifusion. Norepinephrine and epinephrine suppressed basal GH release from goldfish pituitary cells in a reversible and dose-dependent manner. At high doses, a transient rebound of GH release was observed after termination of norepinephrine and epinephrine treatment. In this study, the dose-dependence of adrenergic inhibition on basal GH release was mimicked by the α2 agonists clonidine and UK14304. Basal GH secretion, however, was not affected by the β agonist isoproterenol and α1 agonist methoxamine. In addition, the inhibitory actions of norepinephrine and clonidine on basal GH release were blocked by the α2 antagonists yohimbine and RX821002. The β antagonist propranolol and α1 antagonists prasozin and benoxathian were not effective in this respect. Salmon gonadotropin-releasing hormone (sGnRH) and dopamine, two known GH-releasing factors in fish, stimulated GH release from goldfish pituitary cells and their GH-releasing actions were inhibited by simultaneous treatment with norepinephrine. Furthermore, the GH rebound after norepinephrine treatment was significantly enhanced by prior exposure to sGnRH and this effect was not observed with dopamine treatment. These results, taken together, suggest that in the goldfish adrenergic input at the pituitary level inhibit basal GH release through activation of α2 adrenoreceptors. This α2 inhibitory influence may interact with dopaminergic and GnRH input to regulate GH secretion from goldfish pituitary cells. The `post-inhibition' GH rebound after NE treatment and its sensitivity to sGnRH potentiation may also represent a novel mechanism for GH regulation in fish.
Keywords: growth hormone; α2 adrenoreceptor; norepinephrine; epinephrine; dopamine; gonadotropin-releasing hormone; goldfish pituitary cells
Document Type: Research article
DOI: 10.1046/j.1365-2826.2000.00455.x
Affiliations: 1: Department of Zoology, University of Hong Kong, Hong Kong., 2: Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada.

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Norepinephrine Regulation of Growth Hormone Release from Goldfish Pituitary Cells. II. Intracellular Sites of Action

Authors: Yunker1; Lee2; Wong2; Chang1
Source: Journal of Neuroendocrinology, Volume 12, Number 4, April 2000 , pp. 323-333(11)
Publisher: Blackwell Publishing

Abstract:
Previous results suggest that norepinephrine decreases growth hormone (GH) release in goldfish by means of α-2 adrenoceptor activation. The intracellular mechanisms by which norepinephrine inhibits GH release were examined in the present study using dispersed goldfish pituitary cells. In 2-h static incubation experiments, norepinephrine and the α-2 agonist clonidine decreased basal GH release and the GH responses to stimulation by the dopamine D1 agonist SKF38393 and two native gonadotropin-releasing hormones (GnRH). Norepinephrine also reduced GH responses to the adenylate cyclase activator forskolin, two protein kinase C (PKC) activators (phorbol ester and synthetic diacylglycerol), and two Ca2+ ionophores (ionomycin and A23187). Similarly, norepinephrine applied as a 1-h pulse in cell column perifusion experiments reduced basal GH release and abolished the GH response to a 5-min pulse of arachidonic acid. In goldfish, D1-stimulated GH release is mediated by AC-, arachidonic acid-and Ca2+-dependent pathways, whereas GnRH action is coupled to PKC-and Ca2+-dependent mechanisms. These results suggest that norepinephrine activation of α-2 receptors inhibits ligand-induced GH secretion by actions subsequent to activation of these second messenger cascades. To further characterize norepinephrine mechanisms of action on unstimulated hormone release, the ability of norepinephrine and an α-2 agonist to affect activation of two second messenger cascades under basal conditions was also investigated. Static incubation with clonidine reduced cAMP production in a time-and dose-dependent manner, suggesting that norepinephrine inhibitory action can also be expressed at the level of cAMP production. Resting intracellular free calcium levels in single, identified goldfish somatotropes was unaffected by norepinephrine. However, the inhibitory effects of norepinephrine on basal GH secretion was not observed in the presence of a voltage-sensitive Ca2+ channel agonist. Whether these channels are targets for norepinephrine action on unstimulated GH release requires further investigation.
Keywords: α-2 adrenoceptor action; [Ca2+]i in identified goldfish somatotropes; voltage-sensitive Ca2+ channel; cAMP; protein kinase C; arachidonic acid
Document Type: Research article
DOI: 10.1046/j.1365-2826.2000.00456.x
Affiliations: 1: Department of Biological Sciences, University of Alberta, Edmonton, Alberta, Canada., 2: Department of Zoology, University of Hong Kong, Hong Kong.

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Norepinephrine and epinephrine are hormones released in response to stress. They are a big part of the fight or flight response and affect all sorts of things like increasing blood sugar for energy, vasoconstriction to the organs and vasodilation to the muscles, immunosupression, etc. I think in fish it also causes them to take on too much fluid via the gills and lose solutes (e.g. sodium, chloride, etc).

Norepinephrine and epinephrine reduce growth hormone released from the pituitary gland and there is a rebound effect of releasing more GH afterwards. It means that chronically stressed fish will grow less than they should and that there should be increased growth for a time after an acute stressor goes away.

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