The Effect of Somatostatin on Bombesin-Stimulated Serum Gastrin and Gastric Acid Secretion in Man

Jansen, J. B. M. J.; Lamers, C. B. H. W.

doi:10.1159/000198562

Cited by 11 publications

(2 citation statements)

References 13 publications

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“…19 and it has been suggested that the inhibitory effect of somatostatin on gastric acid secretion is caused by inhibition of gastrin release. Jansen and Lamers,19 however, found that inhibition of gastrin release by somatostatin could not fully account for the inhibition of bombesin stimulated gastric acid secretion, and Vatn et al16 found no changes in basal plasma gastrin during somatostatin infusion.…”

mentioning

confidence: 99%

Is somatostatin a humoral regulator of the endocrine pancreas and gastric acid secretion in man?

Loud¹,

Holst²,

Egense³

et al. 1985

Gut

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SUMMARY The effect of low dose infusions of somatostatin on meal stimulated gastric acid secretion was studied in eight healthy volunteers by intragastric titration after a peptone test meal with radioimmunoassay control of the plasma concentrations of somatostatin and the pancreatic hormones glucagon and insulin. Infusion of somatostatin in a dose of 100 ng/kg/h, resulting in a plasma concentration of 13A4±2 1 pmol/l, inhibited acid secretion significantly, and in a dose of 800 ng/kg/h, with corresponding plasma concentration of 66-5±12-0 pmol/l the acid secretion was virtually abolished. Plasma concentrations of insulin and pancreatic glucagon decreased significantly during infusion of 200 ng/kg/h (24.5±7.5 pmol/l) and glucose concentrations increased. Serum gastrin was only significantly decreased during the highest dose of somatostatin. The range of plasma somatostatin concentrations obtained with the lower doses correspond to reported physiological variations. The results support the concept that somatostatin participates in the hormonal control of the pancreatic endocrine and the acid secretion.The particular localisation and shape of the somatostatin-producing D-cells in the gastric epithelium and the pancreatic islets suggests that somatostatin acts as a paracrine messenger. 1-4 Studies in dogs by Schusdziarra et at5 however, have indicated that somatostatin may act as a true hormone with a regulatory role in the homeostasis of ingested nutrients. Furthermore, studies in different experimental animals613 and human subjects1420 have shown that exogenous somatostatin is a potent inhibitor of gastric acid secretion and of the endocrine pancreas, and it has been suggested that somatostatin participates in the physiological control of these secretions as a hormonal mediator.5 20-21 The reported effects of somatostatin may be pharmacological, however, because plasma concentrations were generally not controlled.The present study deals with the effect of increasing doses of somatostatin on meal stimulated gastrin and gastric acid secretion under immunochemical control of the plasma concentrations of somatostatin. In addition we studied the effect on

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mentioning

confidence: 99%

Is somatostatin a humoral regulator of the endocrine pancreas and gastric acid secretion in man?

Loud¹,

Holst²,

Egense³

et al. 1985

Gut

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“…In man, infusion of bombesin stimulates gastric acid secretion, pancreatic secretion and gallbladder contraction and has an inhibitory effect on gastric emptying and intestinal motor activity 2 . 6 –9 …”

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confidence: 99%

Effect of bombesin on esophageal motility in humans

Masclee¹,

Lam²,

Lamers³

1999

Diseases of the Esophagus

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We have investigated the effect of bombesin on esophageal motility and explored the mechanism of action of bombesin. Eight healthy subjects were studied in random order during intravenous administration of (1) bombesin, (2) bombesin + vagal cholinergic receptor blockade with atropine and (3) bombesin + somatostatin. Lower esophageal sphincter pressure (LESP) and esophageal body motility were recorded continuously by Dent-sleeve manometry. Bombesin significantly (p < 0.01) increased LESP from 20 +/- 2 mmHg to 43 +/- 6 mmHg. Neither atropine nor somatostatin significantly reduced the bombesin-induced increases in LESP. Bombesin significantly (p<0.05) increased peristaltic wave amplitude (from 61 +/- 4 to 105 +/- 9 mmHg) and duration (from 2.9 +/- 0.2 to 4.8 +/- 0.3 s) in the mid and distal part of the esophagus. Neither atropine nor somatostatin significantly reduced the esophageal body motor response to bombesin. In conclusion (1) bombesin significantly increases LESP and affects esophageal body motility by increasing peristaltic wave amplitude and duration and (2) the effect of bombesin on esophageal motility is not dependent on vagal cholinergic mechanisms and is not mediated by the action of gastrointestinal hormones released by bombesin.

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