Dopaminergic control of antral gastrin and somatostatin release.
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Biomedical subjects
Publications and source records attributed to S Efendic.
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Somatostatin, 0.2-1.0 microgram . kg-1 . min-1, was administered i.v. in 5 anesthetized dogs. Following 9-min infusions, hepatic bile output was found to decrease by approximately 50% after a latency of 6 min. The mode of action suggests that somatostatin inhibits hormone-induced bile output.
The effect of short-time somatostatin infusion on gastric and intestinal propulsion of an oral glucose load was examined in healthy subjects by means of a multiple indicator dilution technique. The early gastric emptying rate was enhanced by somatostatin, indicating delayed gastric inhibition. After withdrawal of the somatostatin infusion, the late gastric emptying rate was decreased and the intestinal propagation rate markedly slowed. The effect of long-time somatostatin infusion has to be examined to analyse the nature of the events described.
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The effect of somatostatin was tested on gastrin release induced by electrical vagal stimulation in anaesthetized cats. The antral release of gastrin was determined in the gastric venous outflow by simultaneous recording of gastrin concentration and blood flow. Repeated vagal stimulation at the same frequency and duration caused release of similar amounts of gastrin within the same cat. Infusion of somatostatin, at a rate of 0.5 microng/kg/min, reduced the vagally induced gastrin release to about 40%. Similarly, basal gastrin output was depressed to about 40% of the control values.
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Antibodies to somatostatin, a recently isolated hypothalamic peptide inhibiting growth hormone release, were used in immunohistochemical studies on the gastrointestinal tract. Somatostatin containing cells in the stomach, and somatostatin-containing nerves in the small and large intestine, could be demonstrated. These findings give evidence of a new type of nerve in the gut.
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