Effect of vagus, gastric inhibitory polypeptide, and HCl on gastrin and somatostatin release from perfused pig antrum

Holst, Jens J.; Jensen, Steen Lund; Nielsen, O.B.; Rehfeld, J. F.

doi:10.1152/ajpgi.1983.244.5.g515

Cited by 33 publications

(24 citation statements)

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“…The difference in antral output would not be expected to be due to a wash-out phenomenon of different magnitude in the 2 groups, since the antral vein blood flow increased by the same mea sure in the adrenalectomized animals and in animals with intact adrenals. We may thus conclude, in agreement with in vitro studies [1,14], that the specific effect of vagal stim ulation is an inhibition of somatostatin re lease in the fundic area, and a stimulation in the antral area; the latter, however, is depen dent on the presence of the adrenals.…”

Section: Discussionsupporting

confidence: 91%

“…Somatostatin inhibits gastrin se cretion (for review, see [5]) and gastrin may stimulate somatostatin release [10]. Because of these findings and the intimate relation ship between antral G and D cells, it has been proposed that endogenous somatosta tin exerts a continuous restraint on gastrin release in a paracrine mode [3], Accordingly, it has been shown that gastrin and somatos tatin secretion generally show an inverse re lationship [11][12][13][14], In agreement with this hypothesis, increased pre-stimulatory out puts of somatostatin (during low and high intragastric pH) were associated with signifi cantly decreased gastrin responses to vagal stimulation in the present experiments.…”

Section: Discussionmentioning

confidence: 99%

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Autonomic Nervous Control of Fundic Secretion of Somatostatin and Antral Secretion of Gastrin and Somatostatin in Pigs

Olesen

Sottimano

et al. 1987

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By selective catheterization of gastric veins, we studied the secretion of gastrin and somatostatin from the antrum and of somatostatin from the gastric fundus-corpus region in anaesthetized pigs with or without acute adrenalectomy. The secretion was studied during electrical stimulation of the vagus nerves and the splanchnic nerves and simultaneous irrigation of gastric lumen with fluids of high, low, and neutral pH. The corpus-fundus somatostatin response to vagal stimulation was biphasic with a short-lasting initial increase followed by a lasting inhibition, which was little influenced by intraluminal pH or adrenalectomy. In pigs with intact adrenals, antral somatostatin secretion was increased by vagal stimulation, whereas in adrenalectomized pigs, the effect was inhibitory. The vagally induced inhibition was abolished when the intragastric pH was kept at pH 2. The antral gastrin secretion was strongly stimulated by vagal stimulation. The magnitude of the secretory response was inversely related to the pre-stimulatory somatostatin levels, but not to the nerve stimulation responses. Splanchnic stimulation increased arterial blood pressure and gastric blood flow, but had inconsistent effects on somatostatin and gastrin secretion.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

Autonomic Nervous Control of Fundic Secretion of Somatostatin and Antral Secretion of Gastrin and Somatostatin in Pigs

Olesen

Sottimano

et al. 1987

Digestion

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“…Gastric acidification of the gastric an trum elevated plasma concentrations of so matostatin in man in accordance with pre vious observations in the dog [ 13] and in the pig [44], The concomitant suppression of plasma gastrin and gastric acid secretion is compatible with a physiological role for antrally released somatostatin. Additional sup port is derived from the inverse covariation of plasma somatostatin and gastrin through out individual experiments.…”

Section: Discussionsupporting

confidence: 87%

Interactions between Antral Peptides and Prostaglandin Biosynthesis in Gastric Acid Regulation in Man

Befrits

Uvnäs-Moberg²,

Johansson³

1990

Digestion

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The role of endogenous prostaglandins as modulators of antral hormone release and gastric acid secretion was studied in the intact human stomach. The subjects (n = 9) received indomethacin prior to gastric perfusion at pH > 7 or < 2 and subsequent vagal stimulation. Indomethacin was also tested against parenteral somatostatin (n = 10) and pentagastrin (n = 8). The release of somatostatin into the circulation was biphasic after vagal stimulation, and the plasma levels were inversely proportional to those of plasma gastrin. Acidification of the gastric antrum from pH > 7 to < 2 increased twofold the basal plasma levels of somatostatin (p < 0.05) and suppressed basal and vagally stimulated gastrin release (p < 0.05) and gastric acid secretion (p < 0.05). Indomethacin prior to acidification had little effect in the basal state. Following stimulation the release of somatostatin increased, as indicated by a twofold elevation of somatostatinlike immunoreactivity in the gastric lumen (p < 0.05), but there was less inhibition of plasma gastrin (p < 0.05) and gastric acid secretion (p < 0.05) as compared to acidification alone. During alkaline gastric perfusion, indomethacin increased circulating somatostatin (p < 0.05) levels without affecting plasma gastrin or gastric acid. Indomethacin given against intravenously infused somatostatin (0.1 μg•kg^-1·h^-1) partially reversed the inhibited gastrin response to vagal stimulation without affecting somatostatin-suppressed gastric acid secretion. The effects of indomethacin against pentagastrin were marginal. In conclusion: Gastric acidification in man stimulates plasma release of somatostatin in parallel to suppressing gastrin release and gastric acid secretion. Endogenous prostanoids participate to regulate antral hormone interactions and may have dual actions on antral somatostatin, as negative modulators of release and as mediators of somatostatin effects on the gastrin cell. It is suggested that an unrestricted release of antral somatostatin is reflected in the gastric lumen rather than in the circulation.

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“…In the stomach, it acts as the final common pathway for several reflexes which inhibit gastrin in the antrum, and acid secretion in the corpus. Antral D-cells have apical microvilli and release somatostatin in response to luminal acid [86,87]. They are also activated by fasting [88], when there is no food to buffer the acid.…”

Section: Gastrin and Somatostatin: The Effect Of H Pylorimentioning

confidence: 99%

Helicobacter pylori

Calam¹

1994

Eur J Clin Investigation

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Effect of vagus, gastric inhibitory polypeptide, and HCl on gastrin and somatostatin release from perfused pig antrum

Cited by 33 publications

References 0 publications

Autonomic Nervous Control of Fundic Secretion of Somatostatin and Antral Secretion of Gastrin and Somatostatin in Pigs

Autonomic Nervous Control of Fundic Secretion of Somatostatin and Antral Secretion of Gastrin and Somatostatin in Pigs

Interactions between Antral Peptides and Prostaglandin Biosynthesis in Gastric Acid Regulation in Man

Helicobacter pylori

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