Selective inhibition by somatostatin of cyclic AMP production in rat gastric glands

Gespach, Christian; Dupont, Christophe; Bataille, D.; Rosselin, G

doi:10.1016/0014-5793(80)81126-4

Cited by 56 publications

(8 citation statements)

References 36 publications

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“…The data are supported by animal studies. Selective inhibition by somatostatin of cAMP production in rat gastric glands has been described by Gespach et al [6].…”

Section: Effect O F Pge2 Somatostatin Andmentioning

confidence: 99%

Inhibition by Prostaglandin E<sub>2</sub>, Somatostatin and Secretin of Histamine-Sensitive Adenylate Cyclase in Human Gastric Mucosa

Becker¹,

Ruoff

1982

Digestion

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The effects of prostaglandin E₂ (PGE₂), somatostatin and secretin on gastric mucosal adenylate cyclase (AC) and their interactions with the histamine-sensitive AC were studied using biopsy specimens of normal human gastric mucosa. PGE₂ (10^-7 to 10^-3 mol/l), somatostatin (10^-9 to 10^-5mol/l), secretin (10^-9 to 10^-6mol/l) and histamine (10^-7 to 10^-3mol/l), all stimulated mucosal AC in a concentration-dependent manner. Besides this effect, PGE₂, somatostatin and secretin significantly inhibited the histamine-activated enzyme at concentrations as low as 10^-10 to 10^-7 (PGE₂), 10^-9 to 10^-6 (somatostatin) and 10^-9 to 10^-5 mol/l (secretin). They were more potent than cimetidine which initiated inhibition at concentrations exceeding 10^-7mol/l. The data show that PGE₂, somatostatin and secretin have a dual action on AC: (1) they all activate human gastric AC on their own, and (2) they all inhibit the histamine-sensitive enzyme at the parietal cell level at nanomolar concentrations, thus underlining the concept that hormonal control is essential in the regulation of gastric acid secretion.

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“…The data are supported by animal studies. Selective inhibition by somatostatin of cAMP production in rat gastric glands has been described by Gespach et al [6].…”

Section: Effect O F Pge2 Somatostatin Andmentioning

confidence: 99%

Inhibition by Prostaglandin E<sub>2</sub>, Somatostatin and Secretin of Histamine-Sensitive Adenylate Cyclase in Human Gastric Mucosa

Becker¹,

Ruoff

1982

Digestion

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“…The relatively small effect of somatostatin on cyclic AMP formation is apparently not due to a partial defect in receptor-mediated adenylate cyclase inhibition in cycvariants; inhibition induced by stable GTP analogs and that induced by somatostatin are similar in wild-type and cyc-cells (unpublished data). Decrease of cyclic AMP levels and inhibition of adenylate cyclase by somatostatin have been described in various other cell types (28)(29)(30)(31). The potency of somatostatin to reduce cyclic AMP levels in cyc-cells and to inhibit adenylate cyclase in cycmembranes was in the range of 0.1 to 1 nM with a maximal effect at 10 nM.…”

mentioning

confidence: 85%

Occurrence of a hormone-sensitive inhibitory coupling component of the adenylate cyclase in S49 lymphoma cyc- variants.

Jakobs¹,

Schultz²

1983

Proc. Natl. Acad. Sci. U.S.A.

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The influence of somatostatin was studied on cyclic AMP levels and adenylate cyclase activity in cyc-variants of S49 lymphoma cells. These cells are deficient in the guanine nucleotide site that mediates hormone-induced adenylate cyclase stimulation, but their cyclase can be stimulated by forskolin. Somatostatin maximally decreased the 30 ,LM forskolin-stimulated cyclic AMP levels by 35%. Half-maximal suppression occurred at about 0.1 nM somatostatin. Somatostatin (up to 1 ,LM) had no effect on the 100 ,LM forskolin-stimulated adenylate cyclase activity in cycmembrane preparations when guanine nucleotides were not present. In the presence of GTP, however, which by itself caused a small decrease in activity, somatostatin maximally inhibited the enzyme by 20-25%. GTP was half-maximally effective at O.1 j.M, and half-maximal inhibition by somatostatin was observed at 0.1-1 nM. In the presence of the stable GTP analog guanosine 5'-O-(3-thiotriphosphate) (1 ,uM), which decreased the stimulated activity by about 40% after a short lag period, somatostatin (1 ,uM) did not cause a further decrease in final activity but reduced the lag period by about 50%. The data indicate that membranes of cyc variants contain a regulatory site that mediates both guanine nucleotide and hormone-induced inhibition of the adenylate cyclase and suggest that the mechanisms of activation and inactivation of this inhibitory site are similar to those of the stimulatory component missing in cyc-membranes.

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“…6). Somatostatin has been shown to inhibit intracellular cAMP production in numerous cell types and to block the effect of substances known to act through increases in cAMP (19,29,30,75). It appears to exert these effects by suppression of adenylate cyclase activation (75).…”

Section: Intracellular Mechanisms Of Somatostatin Actionmentioning

confidence: 99%

Somatostatin

Yamada¹,

Chiba²

1989

Comprehensive Physiology

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Selective inhibition by somatostatin of cyclic AMP production in rat gastric glands

Cited by 56 publications

References 36 publications

Inhibition by Prostaglandin E<sub>2</sub>, Somatostatin and Secretin of Histamine-Sensitive Adenylate Cyclase in Human Gastric Mucosa

Inhibition by Prostaglandin E<sub>2</sub>, Somatostatin and Secretin of Histamine-Sensitive Adenylate Cyclase in Human Gastric Mucosa

Occurrence of a hormone-sensitive inhibitory coupling component of the adenylate cyclase in S49 lymphoma cyc- variants.

Somatostatin

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