Involvement of corticotropin-releasing factor and somatostatin in stress-induced inhibition of growth hormone secretion in the rat.
Corticotropin-releasing factor (CRF), which is released into the pituitary portal blood during exposure to noxious stimuli, can act centrally to inhibit GH secretion. We have investigated a possible role of endogenous CRF in mediating the stress-induced inhibition of GH release in the rat. While exposure to electroshocks markedly lowered plasma GH levels measured 20 min later, the central administration of the CRF antagonist alpha-Hel CRF-(9-41) totally abolished the effect of stress. To examine possible mechanisms through which CRF might mediate the inhibitory action of various stimuli on GH secretion, we have administered antisomatostatin (anti-SS) serum to CRF-injected rats and observed that immunoneutralization of endogenous SS blocked the inhibitory action of CRF on basal plasma GH values. Additionally, we have shown that CRF acted centrally to prevent the stimulatory action of both exogenously administered GH-releasing factor and the endogenous GH-releasing factor released by morphine sulfate. These effects were abolished by previous treatment with anti-SS serum. Such observations support the hypothesis that in the rat, endogenous CRF mediates the inhibitory action of noxious stimuli on GH secretion and further suggest that this effect may involve an increased release of endogenous SS.
Rivier
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Vale
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D000818:Animals; D001921:Brain / Q000187:drug effects; D003346:Corticotropin-Releasing Hormone / Q000008:administration & dosage / Q000494:pharmacology*; D004597:Electroshock; D013006:Growth Hormone / Q000097:blood*; D007116:Immunization, Passive; D007276:Injections, Intraventricular; D009020:Morphine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013004:Somatostatin / Q000276:immunology / Q000378:metabolism*; D013312:Stress, Physiological / Q000378:metabolism*
D013004:Somatostatin; D009020:Morphine; D013006:Growth Hormone; D003346:Corticotropin-Releasing Hormone