title: Direct gastrin action on isolated rat parietal cells induces morphological transformations.
abstract: In isolated rat parietal cells, a potentiating effect by gastrin of the stimulatory action of histamine and dibutyryl-cAMP (DBcAMP) on aminopyrine accumulation, an index of the acid formed and trapped by the cells, was recently reported by us (1991, Am. J. Physiol. 261, G621-G627). In the present study, this mechanism of action of gastrin was further investigated. Enriched parietal cells (approximately 65% parietal cells) were incubated under different conditions and processed for electron microscopy. Morphometric analysis of the micrographs revealed that pentagastrin (100 nM) was as efficient as histamine (100 microM) in inducing the formation of vacuolar/canalicular spaces in the parietal cells. In the presence of the histamine H2-receptor antagonist ranitidine, histamine was ineffective but pentagastrin and gastrin-17 (G17) maintained their capacity to induce the morphological transformations. By stimulation with pentagastrin plus histamine, the vacuolar/canalicular volume was 2-fold higher than by stimulation separately with each one of the secretagogues. G-17 (100 nM) alone was ineffective but potentiated the maximal [14C]aminopyrine accumulation obtained with 100 microM histamine in mucosal cells (approximately 25-35% parietal cells). Ranitidine blocked both histamine-and histamine plus G-17-stimulated aminopyrine accumulation. G-17 potentiated also the stimulation by 1 mM dibutyryl-cyclic AMP but this was not inhibited by ranitidine. Pentagastrin (100 nM) increased the basal [14C]glucose oxidation in mucosal cells by 30%. This increase was not blocked by ranitidine which, however, abolished the histamine-stimulated glucose oxidation. Incubation of the cells with pentagastrin plus histamine resulted in a glucose oxidation which equaled the sum of the values obtained by each one of the agents. These results indicate that gastrin, acting directly on the parietal cells, potentiates the action of histamine on aminopyrine accumulation by increasing the vacuolar/canalicular spaces, a process that is reflected in the metabolic activity of the cells. Thus a major effect of gastrin at the parietal cell level appears to be the induction of a morphology which is characteristic of stimulated cells rather than a direct activation of ion-transport mechanisms.
authors.affiliation: Department of Medical and Physiological Chemistry, Uppsala University, Sweden.
authors.forename: Z Q
authors.initials: ZQ
authors.lastname: Li
authors.forename: J L
authors.initials: JL
authors.lastname: Cabero
authors.forename: B O
authors.initials: BO
authors.lastname: Nilsson
authors.forename: S
authors.initials: S
authors.lastname: Mårdh
mesh_terms: D000632:Aminopyrine / Q000378:metabolism; D000818:Animals; D005755:Gastrins / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism; D006632:Histamine / Q000494:pharmacology; D008297:Male; D010295:Parietal Cells, Gastric / Q000187:drug effects* / Q000648:ultrastructure; D011899:Ranitidine / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction
chemical_list: D005755:Gastrins; D000632:Aminopyrine; D006632:Histamine; D011899:Ranitidine; D005947:Glucose