Abstract

The acid secreting cell of the gastric mucosa undergoes a remarkable transition as it is simulated to secrete HCl, electrically, morphologically, and biochemically. It is planned to investigate the electrical events at either surface of the Necturus oxyntic cell by patch clamp methods, using cell attached, excised patch and whole cell recording to monitor channels and membrane expansion that is associated with activation of secretin. Electron microscopy, using acid space dependent probes, will be used in isolated intact of permeable rabbit gastric glands to determine the site of activation of the HK ATPase, and the pathway of retrieval of the enzyme following inhibition of the secretion by receptor antagonists. Intact and permeable parietal cells and derived vesicles will be used to evaluate the changes that must occur in carriers and pumps at either side of the parietal cell in the process of activating acid secretion. With these methods, a model will be derived that integrates the electrophysiology, morphology, and biochemical of the membrane processes involved in the transition from rest to secretion.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project (R01)
Project #
5R01DK040615-02
Application #
3241008
Study Section
General Medicine A Subcommittee 2 (GMA)
Project Start
1988-08-20
Project End
1993-07-31
Budget Start
1989-09-01
Budget End
1990-07-31
Support Year
2
Fiscal Year
1989
Total Cost
Indirect Cost

  Institution

Name
University of California Los Angeles
Department
Type
Schools of Medicine
DUNS #
119132785
City
Los Angeles
State
CA
Country
United States
Zip Code
90095

  Publications

Marcus, E A; Scott, D R (2001) Cell lysis is responsible for the appearance of extracellular urease in Helicobacter pylori. Helicobacter 6:93-9
Pisegna, J R; Ohning, G V; Athmann, C et al. (2000) Role of PACAP1 receptor in regulation of ECL cells and gastric acid secretion by pituitary adenylate cyclase activating peptide. Ann N Y Acad Sci 921:233-41
Munson, K B; Lambrecht, N; Sachs, G (2000) Effects of mutations in M4 of the gastric H+,K+-ATPase on inhibition kinetics of SCH28080. Biochemistry 39:2997-3004
Lambrecht, N; Munson, K; Vagin, O et al. (2000) Comparison of covalent with reversible inhibitor binding sites of the gastric H,K-ATPase by site-directed mutagenesis. J Biol Chem 275:4041-8
Sachs, G; Shin, J M; Munson, K et al. (2000) Review article: the control of gastric acid and Helicobacter pylori eradication. Aliment Pharmacol Ther 14:1383-401
Zeng, N; Athmann, C; Kang, T et al. (1999) PACAP type I receptor activation regulates ECL cells and gastric acid secretion. J Clin Invest 104:1383-91
Zeng, N; Sachs, G (1998) Properties of isolated gastric enterochromaffin-like cells. Yale J Biol Med 71:233-46
Melle-Milovanovic, D; Milovanovic, M; Nagpal, S et al. (1998) Regions of association between the alpha and the beta subunit of the gastric H,K-ATPase. J Biol Chem 273:11075-81
Scott, D R; Weeks, D; Hong, C et al. (1998) The role of internal urease in acid resistance of Helicobacter pylori. Gastroenterology 114:58-70
Scott, D; Weeks, D; Melchers, K et al. (1998) The life and death of Helicobacter pylori. Gut 43 Suppl 1:S56-60

Showing the most recent 10 out of 51 publications