Direct Inhibition of Gastric Acid and Pepsin Secretion by Growth-Hormone Release-Inhibiting Hormone in Cats

Gómez-Pan, A.; Albinus, Margittá; Reed, J. D.; Shaw, B.; Hall, R.; Besser, G. M.; Coy, David H.; Kastin, Abba J.; Schally, Andrew V.

doi:10.1016/s0140-6736(75)91686-4

Cited by 172 publications

(44 citation statements)

References 13 publications

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“…Barros D' Sa et al (1975) and Gomez-Pan et al . (1975) reported that intravenous infusion of somatostatin suppressed the secretion of gastric acid in response to stimuli of acid production and this effect was mediated by a direct action of somatostatin on parietal cells, since this effect was also found during penta gastrin administration.…”

Section: Discussionmentioning

confidence: 98%

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Immunohistochemical demonstration of somatostatin-positive cells in the canine gut.

Ito

Yamada

Kobayashi

1977

Tohoku J. Exp. Med.

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Section: Discussionmentioning

confidence: 98%

“…It has also extra-pituitary properties such as inhibitory action on the secretion of insulin and glucagon from the pancreatic islet (Alberti et al 1973;Gerich et al 1974) and of hydrochloric acid and pepsin from the fundicgland (Bloom et al 1974; Barros D' Sa et al 1975;Gomez-Pan et al 1975).…”

mentioning

confidence: 99%

Immunohistochemical demonstration of somatostatin-positive cells in the canine gut.

Ito

Yamada

Kobayashi

1977

Tohoku J. Exp. Med.

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“…Previous studies showed that gastric acid secretion induced by pentagastrin or hista mine was directly inhibited by somatostatin in cats and dogs (21,22). However, it cannot be concluded from those studies that soma tostatin had a direct inhibitory effect on acid secretion without ruling out its effects on gastric mucosal blood flow (MBF).…”

Section: Discussionmentioning

confidence: 99%

Inhibitory effect of somatostatin on gastric acid secretion in rats.

Nishikawa

Yokotani²,

Fujiwara

1987

Jpn.J.Pharmacol

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Abstract-Effects of somatostatin on parasympathetically induced increases in gastric acid secretion and mucosal blood tlow (MBF) were studied in anesthetized rats with a gastric fistula. Intravenous infusion of small doses of somatostatin (0.1-0.5 ug/kg/min) dose-dependently inhibited the increases in the vagally stimulated gastric acid secretion. Larger doses of somatostatin (0.5-2.5 ,ug/kg/ min) also dose-dependently inhibited the bethanechol-induced gastric acid secre tion. The dose of somatostatin required to inhibit the gastric acid secretion by about 50% of the preinfused control values was 0.25 ,ug/kg/min for vagally stimu lated acid secretion and 2.5 ,cg/kg/min for bethanechol-induced acid secretion. Thus, the inhibitory potency of somatostatin on the vagally stimulated gastric acid secretion was about 10-fold higher than that on bethanechol-induced acid secretion. Somatostatin had no effect on the increase in gastric MBF during vagus nerve stimulation or bethanechol infusion. Pretreatment with indomethacin or phentol amine had no effect on the inhibitory effect of somatostatin on the increase in gastric acid secretion during vagus nerve stimulation or bethanechol infusion. These results suggest that somatostatin exerts an inhibitory effect on gastric acid secretion by acting on the parasympathetic neurons in the gastric wall more than on the structures peripheral to the parasympathetic nerve terminals, and it reduces para sympathetically stimulated gastric acid secretion in rats. This inhibitoty effect of somatostatin on the gastric acid secretion is independent of the changes in the gastric MBF and probably not related to prostaglandin-involved or alpha adreno ceptor-mediated mechanisms.

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“…Somatostatin, another peptide first isolated from brain tissue and subsequently identified in the gastrointestinal tract, has profound effects on this system including potent inhibition of gastric acid and pepsin secretion (Gomez-Pan, Reed, Albinus, Shaw, Hall, Besser, Coy, Kastin & Schally, 1975 (Hirst, Reed, Shaw, Coy & Schally, 1978 TRH, 20 pg kg-' h-1, significantly reduced the gastric acid response to insulin-induced hypoglycaemia during the second hour of infusion ( Figure 3). -Insulin-stimulated pepsin secretion was also reduced by TRH, but this reduction was only significant in two of the six 15 min collection periods ( Figure 3).…”

Section: Introductionmentioning

confidence: 99%

Effects of Thyrotrophin‐releasing Hormone, and Methionine‐enkephalin on Gastric Acid and Pepsin Secretion in the Cat

Gascoigne

Hirst

Reed

et al. 1980

British J Pharmacology

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upon Tyne NEI 7RU1 The effect of intravenous administration of thyrotrophin-releasing hormone (TRH) and methionine-enkephalin on gastric acid and pepsin secretions was investigated in conscious cats prepared with chronic gastric fistulae.2 TRH, 20 jig kg-' h-', did not influence unstimulated gastric acid secretion, nor gastric acid secretion stimulated by submaximal doses of pentagastrin or histamine. Pepsin secretion stimulated by pentagastrin was not influenced by TRH. 3 TRH, 20 pg kg-' h-, significantly reduced the gastric acid and pepsin responses to intravenous infusion of insulin. TRH also significantly reduced the degree of hypoglycaemia seen in response to insulin. TRH, 20 pg kg-' h-V, but not 5 Mg kg-1 h-V, infused alone resulted in a significant hyperglycaemia. 4 It is concluded that the reduction of insulin-stimulated gastric secretion by TRH is not dependent on the hyperglycaemic action of the peptide. The mechanism of action of TRH on insulin-stimulated secretion is discussed with respect to its site of action. 5 Methionine-enkephalin or the potent analogue, D-Ala2, Met-enkephalinamide were without effect on unstimulated gastric secretion, or secretion stimulated by pentagastrin, histamine, and insulin. The opiate receptor antagonist, naloxone, did not significantly alter the gastric acid or pepsin response to insulin. 6 It is concluded that there is no evidence that opiates stimulate oxyntic glands directly, nor that the oxyntic cells may possess high affinity binding sites for opiates, nor that endogenous opiates are involved in the control of gastric secretion.

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Direct Inhibition of Gastric Acid and Pepsin Secretion by Growth-Hormone Release-Inhibiting Hormone in Cats

Cited by 172 publications

References 13 publications

Immunohistochemical demonstration of somatostatin-positive cells in the canine gut.

Immunohistochemical demonstration of somatostatin-positive cells in the canine gut.

Inhibitory effect of somatostatin on gastric acid secretion in rats.

Effects of Thyrotrophin‐releasing Hormone, and Methionine‐enkephalin on Gastric Acid and Pepsin Secretion in the Cat

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