title: [Role of hypothalamic somatostatin in the regulation of growth hormone secretion in the rat (author's transl)].
abstract: Series of studies were performed to elucidate the role of hypothalamic somatostatin in the regulation of growth hormone (GH) release in rats. Somatostatin was determined by a specific radioimmunoassay. In the first series of experiments, the effects of hypophysectomy, thyroidectomy, the administration of hGH and thyroxine on the hypothalamic somatostatin content were examined. Among these treatments, only hypophysectomy resulted in a significant reduction in somatostatin content and none of the rest of treatments altered somatostatin content. These results suggest that somatostatin content in the hypothalamus did rarely change in response to various endocrine treatments when anatomical connections between hypothalamus and pituitary gland were intact. In the second series of experiments, the effects of dopamine, high (K+) and Ca++ on the release of somatostatin from isolated hypothalamic synaptosomes were studied. Dopamine and high (K+) in the media stimulated the release of somatostatin and the latter effect was completely abolished by the removal of Ca++ from the media. The results suggest that dopamine has a role in modulating the release of somatostatin. In the third series, the effects of hypothalamic deafferentation on plasma GH levels and responses to ether stress were examined. Somatostatin content in the hypothalamus was reduced to about 50% in both anterior (AC) and complete deafferented (CC) rats as compared to their respective controls. The mean plasma GH levels were elevated in AC rats and the levels in CC rats were significantly higher than the control. Plasma GH levels 15 min after ether stress reduced significantly in both AC and CC rats, similarly to their respective controls. These findings suggest that the major portion of hypothalamic somatostatin was provided by other regions of the brain, which did not play a role in mediating stress-induced plasma GH reductions, but appeared to be responsible for maintaining basal GH levels.
mesh_terms: D000818:Animals; D002118:Calcium / Q000494:pharmacology; D003714:Denervation; D004298:Dopamine / Q000494:pharmacology; D013006:Growth Hormone / Q000378:metabolism* / Q000494:pharmacology; D007016:Hypophysectomy; D007031:Hypothalamus / Q000032:analysis / Q000378:metabolism*; D066298:In Vitro Techniques; D008297:Male; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D013004:Somatostatin / Q000302:isolation & purification / Q000378:metabolism / Q000502:physiology*; D013312:Stress, Physiological / Q000503:physiopathology; D013965:Thyroidectomy; D013974:Thyroxine / Q000494:pharmacology
chemical_list: D013004:Somatostatin; D013006:Growth Hormone; D013974:Thyroxine; D011188:Potassium; D002118:Calcium; D004298:Dopamine