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Inhibition of acid formation and stimulation of somatostatin release by cholecystokinin-related peptides in rabbit gastric glands
Department of Physiology, Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, Uppsala, Sweden and the Department of Surgery and the Research Center, Karolinska Institute, Huddinge University Hospital, Sweden.
Department of Clinical Chemistry, Academic Hospital, Uppsala, Sweden.
Department of Physiology, Faculty of Veterinary Medicine, Swedish University of Agricultural Sciences, Uppsala, Sweden and the Department of Surgery and the Research Center, Karolinska Institute, Huddinge University Hospital, Sweden.
1989 (English)In: Journal of Physiology, ISSN 0022-3751, E-ISSN 1469-7793, Vol. 419, 765-774 p.Article in journal (Refereed) Published
Abstract [en]

1. The purpose of the present study was to investigate the role of somatostatin in the inhibition of acid production induced by caerulein and cholecystokinin (CCK) in isolated rabbit gastric glands. Acid production was estimated by the aminopyrine technique.

2. Exogenous somatostatin 14 and somatostatin 28 (10(-7) M) reduced to a similar extent the aminopyrine uptake produced by 5 x 10(-5) M-histamine during the course of 40 min incubation.

3. Significant inhibition of histamine-stimulated aminopyrine accumulation occurred at a somatostatin 14 concentration of 10(-9) M.

4. Caerulein and CCK octapeptide (10(-13)-10(-7) M) were found to release somatostatin from isolated gastric glands in a dose-dependent manner. The dose-response relationships for somatostatin release and inhibition of aminopyrine uptake were similar. Thus, the half-maximal dose approximations for somatostatin release and inhibition of aminopyrine uptake were 0.5 and 1.4 x 10(-9) M respectively for CCK octapeptide and 0.9 and 2.5 x 10(-11) M for caerulein. Heptadecapeptide gastrin proved to be a very poor releaser of somatostatin in the system used. The CCK octapeptide-induced somatostatin release was time dependent and the concentrations of somatostatin that accumulated in the incubation medium were similar to those of exogenous somatostatin that were needed to evoke inhibition.

5. The present results support the concept that cholecystokinin inhibits gastric acid secretion by releasing somatostatin from endocrine-like cells in the gastric mucosa. It is suggested that cholecystokinin-related peptides may play a physiological role in inhibiting gastric acid secretion. A similar role for gastrin is not supported by the present study.

Place, publisher, year, edition, pages
1989. Vol. 419, 765-774 p.
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:liu:diva-79780PubMedID: 2576071OAI: oai:DiVA.org:liu-79780DiVA: diva2:544365
Available from: 2012-08-14 Created: 2012-08-14 Last updated: 2017-12-07Bibliographically approved
In thesis
1. In vitro studies on cholecystokinin-induced inhibition of acid formation in gastric glands
Open this publication in new window or tab >>In vitro studies on cholecystokinin-induced inhibition of acid formation in gastric glands
2000 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

The design of methods useful for the preparation of viable glands and cells from the gastric mucosa allowed detailed studies on the mechanisms that regulate gastric acid secretion. The preparation of rabbit gastric glands was the first suitable method to be used and a number of important scientific contributions have been accomplished with this method. Using this method we studied the effect of CCK-like peptides on [14C]aminopyrine accumulation stimulated by histamine, in order to fmd out whether such peptides can inhibit the production of acid in the parietal cell. We also developed a method for the study of viable rat gastric glands that allowed comparative studies in the rat species.

In rabbit gastric glands CCK-like pep tides inhibited histamine stimulated acid formation whereas gastrin peptides were ineffective. The most potent and efficacious peptides were CCK 8 and the cholecystokinetic amphibian decapeptide cemlein reducing the maximal histamine stimulation of aminopyrine accumulation by 35-38%. The concentration of peptide necessary for eliciting inhibition was in the range of that reported to stimulate amylase secretion in similar in vitro experiments on isolated pancreatic acini, representing a well established physiological function of CCK. Analyses of somatostatin content in the incubation medium revealed that biologically active concentrations of endogenous somatostatin were released into the incubation medium. The rate of somatostatin release increased after CCK 8 or cemlein was added, whereas with G 17, the concentration of somatostatin remained unchanged. In further experiments performed with rabbit mucosal cells prepared from the gastric glands, it was demonstrated that the inhibitory property of CCK 8 only was apparent if a sufficient amount of endocrine cells were present during incubation. In highly purified fractions of parietal cells, however, a small stimulatory effect appeared, a finding that is consistent with similar capacity of gastrin and CCK stimulating the CCK2 receptors present on the parietal cell.

A method useful for the study of rat gastric glands was developed. The viability of the rat gastric glands appeared excellent as judged by morphological characterisation and functional assessment by means of [14C]aminopyrine accumulation. Upon stimulation with a high dose of histamine the production of acid increased 5-fold over basal. Pentagastrin and CCK 8 were ineffective stimulators per se, but in combination with histamine a marked potentiation occurred. Somatostatin effectively inhibited histamine-stimulated acid formation both in rabbit and rat gastric glands.

In conclusion, CCK-like peptides inhibit histamine stimulated acid formation in gastric glands prepared from rabbit. The inhibition is mediated in a paracrine-like mode via the release of endogenous somatostatin. A method useful for the study of viable rat gastric glands was developed. In contrast to rabbit gastric glands, CCK 8 potentiated histamine stimulation in rat glands.

Place, publisher, year, edition, pages
Linköping: Linköpings universitet, 2000. 51 p.
Series
Linköping University Medical Dissertations, ISSN 0345-0082 ; 639
National Category
Medical and Health Sciences
Identifiers
urn:nbn:se:liu:diva-25629 (URN)10000 (Local ID)91-7219-740-4 (ISBN)10000 (Archive number)10000 (OAI)
Public defence
2000-11-13, Berzeliussalen, Hälsouniversitetet, Linköping, 13:00 (Swedish)
Available from: 2009-10-08 Created: 2009-10-08 Last updated: 2012-08-14Bibliographically approved

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