Pertussis toxin reverses prostaglandin E2- and somatostatin-induced inhibition of rat parietal cell H+-production

Somatostatin sst2 receptor‐mediated inhibition of parietal cell function in rat isolated gastric mucosa

“…The ability of SRIF-14 to inhibit gastric acid secretion is well documented and involves both a direct effect on gastric parietal cells and an indirect effect involving inhibition of histamine release from gastric ECL cells (Park et al, 1987;Schmidtler et al, 1992;Prinz et al, 1994). in the stomach (Bruno et al, 1993;Raulf et al, 1994), the functional significance of each receptor subtype is still unknown.…”

“…Although the mRNA for sst2 receptors has been identified on ECL cells, the ability of SRIF to inhibit acid secretion induced by the H2 receptor agonist, dimaprit, in the present study, suggests that SRIF receptors are also located on rat parietal cells. Indeed SRIF-14 has been shown to inhibit histamine and forskolin stimulated acid secretion in an enriched isolated parietal cell preparation of the rat (Schmidtler et al, 1992). However, the identity of the SRIF receptor involved is unknown.…”

“…Preincubation with BIM-23056 (1 gM) had no effect on SRIF-induced inhibition of dimaprit-induced gastric acid secretion (Figure 3). The ability of SRIF-14 to inhibit gastric acid secretion is well documented and involves both a direct effect on gastric parietal cells and an indirect effect involving inhibition of histamine release from gastric ECL cells (Park et al, 1987;Schmidtler et al, 1992;Prinz et al, 1994 experiments.…”

“…Immunohistochemical studies have demonstrated SRIF-like immunoreactivity in large amounts in the stomach (Arimura et al, 1975), where it is localised predominantly in the fundic and antral mucosa (Penmann et al, 1983) and where it can inhibit gastric acid and pepsinogen secretion in response to stimulation by pentagastrin (Rossowski et al, 1994;Tanaka & Tani, 1994). The ability of SRIF-14 to inhibit acid secretion has long been known and may involve direct effects mediated by SRIF receptors located on parietal cells, as well as indirect effects on histamine release from enterochromaffin-like (ECL) cells (Park et al, 1987;Schmidtler et al, 1992;Payne & Gerber, 1992;Prinz et al, 1994).…”

Revisiting the parietal cell

“…Somatostatin, which is known to be released by D cells in the antrum and fundus upon stimulation by cholecystokinin (CCK) and vasoactive intestinal peptide (VIP) (9,163), has a direct effect on parietal cells by lowering intracellular cAMP concentrations via an inhibitory G protein that attenuates adenylyl cyclase activity (108). Inhibition of the G protein by pertussis toxin made this process reversible and rendered the parietal cells resistant to the effects of somatostatin (108,130). A somatostatin receptor (SSTR 2 ) knockout model has further shown an increase in acid output in response to vagal and gastrin stimulation (165).…”