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  • American Physiological Society  (4)
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  • American Physiological Society  (4)
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  • 1
    Online Resource
    Online Resource
    American Physiological Society ; 1991
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 260, No. 6 ( 1991-06-01), p. G925-G928
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 260, No. 6 ( 1991-06-01), p. G925-G928
    Abstract: To study the interdependence between gastric histamine release and acid secretion, we examined the effects of gastrin-(1-17) [G-(1-17)] or cholecystokinin-(1-33) [CCK-(1-33)] alone or combined with the gastrin (CCK-B) antagonist L365,260 or the CCK-A antagonist L364,718 in the isolated vascularly perfused rat stomach. G-(1-17) and CCK-(1-33) gave concentration-dependent increases in acid secretion and histamine release. Gastrin or CCK-A antagonist alone did not stimulate histamine release or acid secretion. Maximally G-(1-17) or CCK-(1-33) stimulated histamine release and acid secretion was unchanged by the CCK-A antagonist, while the gastrin antagonist induced a parallel and concentration-dependent decrease in stimulated histamine and acid secretion. We conclude that G-(1-17) and CCK-(1-33) stimulate histamine and acid secretion by a CCK-B (gastrin) receptor. The present results indicate that gastrin, at least in this species, stimulates acid secretion by releasing histamine.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1991
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Location Call Number Limitation Availability
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  • 2
    Online Resource
    Online Resource
    American Physiological Society ; 1994
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 267, No. 2 ( 1994-08-01), p. G254-G258
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 267, No. 2 ( 1994-08-01), p. G254-G258
    Abstract: Gastrin release histamine from the oxyntic mucosa, stimulates the enzymatic activity of histidine decarboxylase (HDC), increases HDC mRNA abundance, and has a trophic effect on the enterochromaffin-like (ECL) cell. In the present study, we examined the effect of exogenous gastrin on HDC activity and mRNA and the time scale of increase and decline of HDC activity and mRNA. Rats received intravenous infusion of gastrin-(1-17) in different doses or periods of time. Oxyntic mucosal HDC activity and mRNA abundance increased significantly with serum gastrin concentrations in the physiological range. The onset of response was rapid and maximal for both parameters after 2 h. Poststimulatory decrease was maximal 2 h after cessation of gastrin infusion. Those observations suggest that HDC enzymatic activity and mRNA abundance are important in meal-to-meal regulation of gastric secretion. Furthermore, HDC enzymatic activity and mRNA abundance varied in parallel, indicating that HDC mRNA abundance is important in the overall regulation of gastric mucosal HDC activity.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1994
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Location Call Number Limitation Availability
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  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1995
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 269, No. 4 ( 1995-10-01), p. G542-G547
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 269, No. 4 ( 1995-10-01), p. G542-G547
    Abstract: Somatostatin modulates both endocrine and exocrine functions in the gastric mucosa, where three of the five cloned somatostatin receptors are present. This study examines changes in somatostatin receptor (SSTR) mRNA abundance during fasting, feeding, and profound acid inhibition with omeprazole. Serum gastrin as well as somatostatin and SSTR mRNA abundances were measured in antrum and corpus. In Northern blots of corpus RNA, the SSTR2 probe hybridized with two previously reported species of mRNA (2.4 and 2.8 kb); in addition, a weak previously unreported 1.6-kb band was detected. In antrum, the 1.6-kb band dominated. Fasting increased antral somatostatin mRNA from 100 +/- 8 to 161 +/- 24% and SSTR mRNA from 100 +/- 10 to 179 +/- 14% (P 〈 0.05). Omeprazole reduced antral somatostatin mRNA to 34 +/- 4% of control (P 〈 0.05) and elevated SSTR mRNA to 135 +/- 5% of control (P 〈 0.01). Omeprazole treatment reduced corpus somatostatin mRNA to 59 +/- 5% (P 〈 0.05), and elevated SSTR mRNA to 140 +/- 3% of control (P 〈 0.01). The results therefore indicate that a novel SSTR mRNA subtype exists in the stomach and predominates in the antrum. The abundance of this SSTR mRNA is upregulated by both fasting and achlorhydria; conditions that increase or decrease endogenous antral somatostatin, respectively.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1995
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Location Call Number Limitation Availability
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  • 4
    Online Resource
    Online Resource
    American Physiological Society ; 1993
    In:  American Journal of Physiology-Gastrointestinal and Liver Physiology Vol. 264, No. 1 ( 1993-01-01), p. G51-G56
    In: American Journal of Physiology-Gastrointestinal and Liver Physiology, American Physiological Society, Vol. 264, No. 1 ( 1993-01-01), p. G51-G56
    Abstract: This study examined the second messenger system responsible for gastrin-induced histamine release from the rat stomach. We examined the effect of different concentrations of ionized calcium, the calcium-channel blockers verapamil and nicardipine, and the intracellular calcium-chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxymethyl ester (BAPTA/AM) on gastrin-stimulated histamine release in the totally isolated vascularly perfused rat stomach. Moreover, the effect on baseline histamine release of caffeine as well as of forskolin and 3-isobutyl-1-methylxanthine (IBMX) was tested. Gastrin induced an immediate 10- to 15-fold increase in venous histamine. Perfusate ionized calcium in the 0.25-1.25 mM range did not affect histamine release; histamine release was attenuated by the 0.00 and 1.75 mM calcium concentrations. Verapamil, nicardipine, and BAPTA/AM inhibited gastrin-stimulated histamine release. Caffeine stimulated the release, whereas forskolin and IBMX had no effect. We conclude that gastrin-induced histamine release from the rat stomach is mediated by calcium, probably both from the intracellular pool and by transmembrane flux from the extracellular space.
    Type of Medium: Online Resource
    ISSN: 0193-1857 , 1522-1547
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1993
    detail.hit.zdb_id: 1477329-6
    SSG: 12
    Location Call Number Limitation Availability
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