Effect of PACAP on gastric acid secretion in rats

Mungan, Zeynel; Hammer, Robert A.; Akarca, Ulus Salih; Kobashi, Gén; Ertan, Atilla; Arimura, Akira

doi:10.1016/0196-9781(95)00083-v

Cited by 33 publications

(27 citation statements)

References 18 publications

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“…Previous work had shown either no effect or inhibition of acid secretion by intravenous administration of PACAP (18,19). Given the effect of this peptide on ECL cell function as shown above, it seemed possible that the stimulatory effect of PACAP was masked by stimulation of fundic D cells by the injected hormone, perhaps at a VIP receptor as suggested by the results from our tests on D cells.…”

Section: Stimulation Of Ecl Histamine Release By Pacapmentioning

confidence: 54%

“…The previously described in vivo data (18,19) showing inhibition of gastrin-stimulated acid secretion could be a result of D-cell stimulation by injected PACAP. To determine the effect of PACAP and VIP on D cells, gastric D cells were isolated, and calcium signals and somatostatin release were measured in response to PACAP-27 and VIP.…”

Section: Stimulation Of Ecl Histamine Release By Pacapmentioning

confidence: 99%

“…Peripheral injection has been variously reported to either have no effect or to inhibit gastrin-stimulated acid secretion. This makes its candidacy as a mediator of stimulation of gastric acid secretion questionable (18,19). Like gastrin, PACAP stimulates growth of ECL cells in vitro (20).…”

Section: Introductionmentioning

confidence: 99%

“…Like gastrin, PACAP stimulates growth of ECL cells in vitro (20). We are therefore faced with the paradox of an effective in vitro stimulant of gastric ECL cell function acting as an inhibitor of acid secretion in vivo (18,19).…”

Section: Introductionmentioning

confidence: 99%

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PACAP type I receptor activation regulates ECL cells and gastric acid secretion

Zeng¹,

Athmann²,

Tai³

et al. 1999

J. Clin. Invest.

116

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The regulation of acid secretion has been divided into cephalic and peripheral (gastric and intestinal) phases (1). The cephalic phase of gastric acid secretion originates in the central nervous system and impacts the hypothalamus; signals travel via the vagus nerve to the myenteric plexuses of the gastric mucosa. In the succeeding neural network, a variety of secondary neurons signal the gastric fundic and antral epithelia to influence gastric acid secretion by either primary or secondary action, namely, direct effects on parietal cells or gastric epithelial endocrine cells. The peripheral phase of acid secretion regulation involves local signaling within a variety of endocrine cells, transmitting regulatory information to the secretory cells of the gastric mucosa; the peripheral phase is more limited than the cephalic phase in terms of the possible mediators involved (2). Studies of isolated gastric endocrine cells have proved useful in defining the interactions of various signals in the regulation of gastric acid secretion, but such studies must be placed in context when considering their physiological implications. The isolated rabbit gastric gland is a more integrated model than that provided by isolated cells.With the isolation and purification (to between 85% and 95%) of functional enterochromaffin-like (ECL) cells from the rat gastric mucosa, a variety of receptors has been defined on this cell type. This has been done by measurement of calcium signals under superfusion conditions using video microscopy, and by histamine or pancreostatin release by radioimmunoassay under static conditions (3-5). When histamine release is measured in a static system, cross-talk is a problem. Superfusion of isolated, enriched ECL cells while measuring responses of intracellular calcium [Ca 2+ ] i eliminates cross-talk between possible contaminating gastric endocrine cells. Nevertheless, few (if any) inconsistencies have been found between the results of video-imaging and release measurements in this particular preparation. In this preparation, there are less than 2% D cells, and the addition of somatostatin antibody has not affected either calcium signaling or histamine release in response to a variety of agonists (3, 4).Histamine, released from ECL cells, is the most important direct stimulant of acid secretion, as shown by the broad efficacy of histamine-2 receptor antagonists as full inhibitors of gastrin and partial inhibitors of vagally stimulated acid secretion (6). The involvement of ECL cells in mediation of the cephalic (neural) phase of gastric acid secretion has been less clear. The atropine sensitivity of cephalic stimulation of acid secretion pointed

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Section: Stimulation Of Ecl Histamine Release By Pacapmentioning

confidence: 54%

Section: Stimulation Of Ecl Histamine Release By Pacapmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

PACAP type I receptor activation regulates ECL cells and gastric acid secretion

Zeng¹,

Athmann²,

Tai³

et al. 1999

J. Clin. Invest.

116

View full text Add to dashboard Cite

show abstract

“…Pituitary adenylate cyclase-activating polypeptide (PACAP) has become an increasingly likely candidate since its recent identification in gastric enteric neurons (6) and the discovery of its ability to stimulate histamine secretion (7,8) and proliferation by ECL cells in culture (9). However, peripheral injection of PACAP has been shown to inhibit gastrin-stimulated acid secretion in vivo (10). This finding may be understood as an artifact of peripheral injection: other cell types within the gastric gland might give rise to an opposing (but perhaps nonphysiologic) response to PACAP.…”

Section: Commentarymentioning

confidence: 99%