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dc.contributor.authorGrabau, B Jen
dc.contributor.authorZavros, Yen
dc.contributor.authorHardy, Kenneth Johnen
dc.contributor.authorShulkes, Arthuren
dc.date.accessioned2015-05-16T03:31:20Z
dc.date.available2015-05-16T03:31:20Z
dc.date.issued1999-02-01en
dc.identifier.citationEndocrinology; 140(2): 603-8en
dc.identifier.govdoc9927283en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/13645en
dc.description.abstractGastric somatostatin (SRIF) regulates gastric acidity by inhibiting gastric acid and gastrin secretion. SRIF secretion is increased by gastric acidity and also directly by regulators of gastric acid secretion such as gastrin. This direct effect has not been described in the developing animal, nor have the roles of intermediaries such as histamine and gastric acidity been defined. The present study aimed to establish the regulatory role of gastrin and histamine during development on SRIF secretion and also to determine whether the effects of gastrin and histamine are independent of gastric pH. Pentagastrin and histamine were infused on separate occasions into fetal sheep, newborn lambs, and 28-day-old lambs. To determine the roles of endogenous histamine and gastric pH, ranitidine (a histamine-2 receptor antagonist) and omeprazole (a H+/K+ ATPase inhibitor) were coinfused with the agonists. Plasma SRIF and gastrin concentrations were measured by RIA. Pentagastrin stimulated SRIF secretion in the fetus after 131 days of gestation (term is 147 days), whereas stimulation by histamine was effective only after birth. The SRIF stimulatory effect of pentagastrin in 28-day-old lambs was abolished by ranitidine, which also reduced this effect in the adult sheep. This inhibitory effect of ranitidine was shown to be a result of blockade of stimulatory H2 receptors, because in the adult blockade of acid secretion with omeprazole failed to attenuate the response of histamine. These results indicate that in the fetus, gastrin receptors, but not histamine receptors, are functionally involved in the stimulation of SRIF secretion. After birth, both gastrin and histamine stimulate SRIF, but the effect of gastrin is mediated at least in part by the release of endogenous histamine. These responses occur independently of changes in gastric acidity, supporting the concept of a direct negative feedback between SRIF and gastrin.en
dc.language.isoenen
dc.subject.otherAging.metabolismen
dc.subject.otherAnimalsen
dc.subject.otherAnimals, Newborn.growth & development.metabolismen
dc.subject.otherDrug Combinationsen
dc.subject.otherEmbryonic and Fetal Development.physiologyen
dc.subject.otherFemaleen
dc.subject.otherFetus.physiologyen
dc.subject.otherGastric Mucosa.drug effects.secretionen
dc.subject.otherGastrins.secretionen
dc.subject.otherHistamine.pharmacologyen
dc.subject.otherMaleen
dc.subject.otherOmeprazole.pharmacologyen
dc.subject.otherPentagastrin.pharmacologyen
dc.subject.otherRanitidine.pharmacologyen
dc.subject.otherSheep.embryologyen
dc.subject.otherSomatostatin.secretionen
dc.subject.otherStomach.embryology.growth & developmenten
dc.subject.otherTime Factorsen
dc.titleDevelopmental regulation of gastric somatostatin secretion in the sheep.en
dc.typeJournal Articleen
dc.identifier.journaltitleEndocrinologyen
dc.identifier.affiliationDepartment of Surgery, University of Melbourne, Austin, Victoria, Australia.en
dc.identifier.doi10.1210/endo.140.2.6497en
dc.description.pages603-8en
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/9927283en
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