Basic–Alimentary TractNitric oxide regulates the release of somatostatin from cultured gastric rabbit primary D-cells☆,☆☆
Section snippets
Chemicals
Collagenase (type 1 and type H), ethylenediaminetetraacetic acid (EDTA), dithiothreitol (DTT), deoxyribonuclease (DNAse), bovine serum albumin (BSA), glutamine, HEPES, streptomycin sulphate, gentamicin sulphate, penicillin, hydrocortisone, bovine insulin, fetal calf serum (FCS), gelatin, CCK8, sodium nitroprusside (SNP), sodium nitrite, L-arginine, L-lysine, epinephrine, 3-aminobenzamide and lactate dehydrogenase (LDH) diagnostic kit were all purchased from Sigma Chemicals (Poole, Dorset,
Immunocytochemistry
At the time of experimentation, 45% of cells in the preparation were D-cells (Figure 1).The rest of the cells were mostly mucous cells: Thirty percent of the cells in the preparation were PAS-positive.
Effects of amino acids
L-arginine, 1 mmol/L, significantly stimulated the release of somatostatin in the D-cell preparation in the presence of CCK8. Hormone release
Discussion
The present studies show that L-arginine-stimulated somatostatin release is prevented by NOS inhibitors and that NO donors release somatostatin. We found evidence that ADP ribosylation is involved in the effect of NO on D-cells but no evidence that cGMP is involved. The stimulatory effect of NO on D-cells occurred over 2 hours, but preincubation with a slow-releasing NO donor for 12 hours suppressed the subsequent 2-hour response of D-cells to stimuli.
Although major advances have been made in
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2012, European Journal of PharmacologyCitation Excerpt :Moreover, the antihistaminic activity of TQ (Marozzi et al., 1970; Kanter et al., 2006) offers another explanation for reducing the acid output, besides the reinstatement of NO, shown in the present work (Tanaka et al., 2001). NO suppresses histamine release; hence, acid output, by increasing cGMP (Kato et al., 1998) and/or enhancing somatostatin release from D cells (Arebi et al., 2002). TQ also reduced peptic activity of gastric juice as shown in this study, possibly via inhibition of histamine release (Kanter et al., 2006), and/or decreased gastric acidity, which attenuates the acid-stimulated activation of pepsinogens to the active pepsin in the gastric juice.
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Address requests for reprints to: Naila Arebi, M.D., Gastroenterology, Hammersmith Hospital, London W12 0NN, United Kingdom. e-mail: [email protected]; fax: (440) 20-8749-3436.
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Supported by a grant from the Astra Foundation (to Z.H.) and from the Digestive Diseases Foundation (to P.B.).