title: Physiological role of somatostatin-mediated autofeedback regulation for growth hormone: importance of growth hormone in triggering somatostatin release during a trough period of pulsatile growth hormone release in conscious male rats.
abstract: In mammals including human, it is generally accepted that growth hormone (GH) can regulate its own secretion through an autofeedback mechanism in which somatostatin (SRIF) may be involved. To explore a physiological role of SRIF-mediated GH autoregulation, the effect of exogenous human GH administration on plasma rat GH response to [D-Ala2, Nle27]-human GH-releasing hormone-(1-28)-agmatine (hGHRH-analog), which does not crossreact with anti-rat GH-releasing hormone gamma-globulin (GHRH-Ab), was examined in conscious male rats treated with GHRH-Ab in the absence and presence of anti-SRIF gamma-globulin (SRIF-Ab). Enhanced SRIF release during a trough period of natural pulsatile GH secretion, suggested by the blunted GH response to exogenous hGHRH-analog, no longer occurred when major GH secretory bursts were abolished by GHRH-Ab treatment. On the other hand, when hGH was administered in GHRH-Ab-treated rats so as to simulate the quantity and dynamic change of GH in hypophysial portal circulation in rats exhibiting pulsatile GH secretion, hGHRH-analog-induced GH rises were significantly suppressed during the period corresponding to a GH trough. This suppression was completely prevented by simultaneous treatment with SRIF-Ab. Furthermore, administration of bovine GH, but not ovine prolactin, resulted in significant suppression of hGHRH-analog-provoked GH rises. These findings suggest that enhanced SRIF release during a trough period of spontaneous GH secretory rhythm is induced by the preceding GH secretory burst, and also suggest a possible role for SRIF-mediated GH autoregulation in a physiological state.
authors.affiliation: Department of Medicine, Kobe University School of Medicine, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Sato
authors.forename: K
authors.initials: K
authors.lastname: Chihara
authors.forename: T
authors.initials: T
authors.lastname: Kita
authors.forename: Y
authors.initials: Y
authors.lastname: Kashio
authors.forename: Y
authors.initials: Y
authors.lastname: Okimura
authors.forename: N
authors.initials: N
authors.lastname: Kitajima
authors.forename: T
authors.initials: T
authors.lastname: Fujita
mesh_terms: D000376:Agmatine / Q000494:pharmacology*; D000818:Animals; D003429:Cross Reactions; D004305:Dose-Response Relationship, Drug; D005246:Feedback; D013006:Growth Hormone / Q000031:analogs & derivatives / Q000097:blood / Q000378:metabolism* / Q000494:pharmacology; D013007:Growth Hormone-Releasing Hormone / Q000031:analogs & derivatives* / Q000276:immunology / Q000494:pharmacology; D006146:Guanidines / Q000494:pharmacology*; D006706:Homeostasis; D019382:Human Growth Hormone; D007106:Immune Sera / Q000008:administration & dosage / Q000276:immunology; D008297:Male; D010507:Periodicity; D051381:Rats; D011919:Rats, Inbred Strains; D017337:Sermorelin / Q000031:analogs & derivatives*; D013004:Somatostatin / Q000276:immunology / Q000378:metabolism / Q000502:physiology*
chemical_list: D006146:Guanidines; D007106:Immune Sera; C052685:DBO 29; D019382:Human Growth Hormone; D013004:Somatostatin; D000376:Agmatine; D017337:Sermorelin; D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone