Cellular Control of Pepsinogen Secretion

Hersey, S. J.; Norris, S. H.; Gibert, Anne J.

doi:10.1146/annurev.ph.46.030184.002141

Cited by 18 publications

(6 citation statements)

References 18 publications

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“…Even today we lack a full understanding of the specific neural and hormonal factors responsible for pepsinogen secretion, of the intracellular mechanisms of stimulus-secretion coupling and of the mechanism of release of the granular contents, as discussed in detail by Hersey et al (1984). By contrast there is a considerable literature on the biochemistry of pepsins; it is apparent that many species are able to secrete several forms with different pH optima, which correspond to the need for activity from near neutrality immediately after a meal to the low pH found several hours later.…”

Section: P E P S I N O G E N S E C R E T I O Nmentioning

confidence: 99%

Nutritional Regulation of Gastric Secretion, Digestion and Emptying

Low¹

1990

Nutr. Res. Rev.

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Section: P E P S I N O G E N S E C R E T I O Nmentioning

confidence: 99%

Nutritional Regulation of Gastric Secretion, Digestion and Emptying

Low¹

1990

Nutr. Res. Rev.

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“…Parietal cells secrete HCI, whereas chief cells secrete pepsinogen. Cholinergic stimulation induces both cell types to secrete (Berglindh et al, 1980;Koelz et al, 1982) through a Ca-regulated pathway (Hersey et al, 1984;Brown, 1986, 1989;Negulescu et al, 1989). Agents that elevate adenosine 3',5'-cyclic monophosphate (cAMP) have also been shown to be extremely potent stimulants of acid secretion.…”

Section: Introductionmentioning

confidence: 99%

Fluorescence measurements of cytosolic free Na concentration, influx and efflux in gastric cells.

et al. 1990

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Regulation of cytosolic free Na (Na-) was measured in isolated rabbit gastric glands with the use of a recently developed fluorescent indicator for sodium, SBFI. Intracellular loading of the indicator was achieved by incubation with an acetoxymethyl ester of the dye. Digital imaging of fluorescence was used to monitor Na1 in both acid-secreting parietal cells and enzyme-secreting chief cells within intact glands. In situ calibration of Na; with ionophores indicated that SBFI fluorescence (345/385 nm excitation ratio) could resolve 2 mM changes in Nal and was relatively insensitive to changes in K or pH. Measurements on intact glands showed that basal Nal was 8.5 ± 2.2 mM in parietal cells and 9.2 ± 3 mM in chief cells. Estimates of Na influx and efflux were made by measuring rates of Na, change after inactivation or reactivation of the Na/K ATPase in a rapid perfusion system. Na/ K ATPase inhibition resulting from the removal of extracellular K (K) caused Na1 to increase at 3.2 ± 1.5 mM/min and 3.5 ± 2.7 mM/min in parietal and chief cells, respectively. Na buffering was found to be negligible. Addition of 5 mM K. and removal of extracellular Na (Na4) caused Na1 to decrease rapidly toward 0 mM Na. By subtracting passive Na efflux under these conditions (the rate at which Na1 decreased in Na-free solution containing ouabain), an activation curve (dNaJNaJ for the Na/K ATPase was calculated.The pump demonstrated the greatest sensitivity between 5 and 20 mM Nal. At 37°C the pump rate was <3 mM/min at 5 mM Na1 and 26 mM/min at 25 mM Nal, indicating that the pump has a great ability to respond to changes in Nal in this range. Carbachol, which stimulates secretion from both cell types, was found to stimulate Na influx in both cell types, but did not have detectable effects on Na efflux. dbcAMP+IBMX, potent stimulants of acid secretion, had no effect on Na metabolism.

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“…CCK-8 was found to be an effective stimulus for pepsinogen secretion in gastric glands (Hersey et al 1984, Yahav et al 1986). The related, and presumed physiologically active peptide, gastrin, is less potent than CCK-8.…”

Section: Discussionmentioning

confidence: 99%

“…I the gastrointestinal tract (Yonoszai & Rainshaw 1973). T h e rapid growth of the stomach which occurs around the third post-natal week is associated with functional maturation of acid and pepsin secretion (Samloff 1971, Hirschowitz 1976, Ikezaki & Johnson 1983, Hersey et al 1984, Seidel & Johnson 1984, Johnson 1985.…”

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confidence: 99%

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The effect of post‐natal malnutrition on pepsinogen secretion receptors in weanling rats

Yahav

Fradkin

Diver-Haber

et al. 1990

Acta Physiologica Scandinavica

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Post-natal malnutrition was induced in rats using the expanded litter model. Pepsinogen secretion of isolated gastric glands in response to several secretagogues was measured. Malnourished 19-day-old pups showed no response to carbachol, CCK-8, gastrin, secretin and ionophore A23187 compared to well-nourished animals, but showed comparable secretion of pepsinogen after stimulation with dibutyryl cAMP (DiBcAMP). Hydrocortisone treatment for 48 h caused increased pepsinogen accumulation and elevated pepsinogen secretory responsiveness to carbachol and secretin of gastric glands isolated from post-natal malnourished pups. Our results indicate that isolated gastric glands obtained from well-nourished rat possess two functionally distinct receptors for gastrin and C-terminal fragment of CCK. Our study supports the concept that in malnourished rats there is a decreased number of binding sites or/and some post-receptor defects. Pepsinogen release mechanisms remain unaffected.

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Cellular Control of Pepsinogen Secretion

Cited by 18 publications

References 18 publications

Nutritional Regulation of Gastric Secretion, Digestion and Emptying

Nutritional Regulation of Gastric Secretion, Digestion and Emptying

Fluorescence measurements of cytosolic free Na concentration, influx and efflux in gastric cells.

The effect of post‐natal malnutrition on pepsinogen secretion receptors in weanling rats

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