A comparative molecular--pharmacological study of drugs inhibiting Na+--K+-dependent ATPase separated from human gastric fundic mucosa. (One receptor system and more drugs).
Acta Med Acad Sci Hung, 1979;36(4):459-66.
Mózsik G, Kutas J, Nagy L, Tárnok F
PMID: 233402
Abstract
The inhibitory effects of atropine, epinephrine, cyclic 3', 5'-AMP (cAMP), the prostaglandins E1 (PGE1) and E2 (PGE2) pentagastrin, histamine and ouabain have been studied on the activity of Na+--K+-dependent ATPase obtained from human gastric fundic mucosa. This study compares the sensitivity of the enzyme to a variety of drugs, applying the law of one receptor and more drugs. It was found that (1) the doses of drugs necessary to produce 50% inhibition to Na+--K+-dependent ATPase activity (affinity, pD2 value) significantly differ from each other C (atropine, 9.50; epinephrine, 8.60; cAMP: 11.30; PGE1, 9.30; PGE2, 9.45; pentagastrin, 9.45; histamine, 9.70 and ouabain, 9.50); (2) the intrinsic activities of drugs to Na+--K+-dependent, ATPase in comparison with ouabain (alpha=1.00) differ: atropine, PGE1, PGE2 and histamine, 1.00; pentagastrin, 0.87; cAMP, 0.48 and epinephrine, 0.41; (3) the inhibitory effects of different drugs, on Na+--K+-dependent ATPase system, depend on the magnitude of enzyme activity from human gastric fundic mucosa. It has been concluded that (1) the sensitivity of these drugs to the Na+--K+-dependent ATPase system and to the adenylate cyclase system, both obtained from human gastric mucosa, significantly differs from each other; (2) the main effect of pentagastrin and histamine on human gastric secretory function differs from the function of Na+--K+-dependent ATPase system; (3) the role of Na+--K+-dependent ATPase system and of adenylate cyclase can be separated pharmacologically from the point of view of human gastric H+ secretion.
MeSH terms
Atropine; Cyclic AMP; Dose-Response Relationship, Drug; Epinephrine; Gastric Mucosa; Histamine; Humans; Ouabain; Pentagastrin; Prostaglandins E; Sodium-Potassium-Exchanging ATPase
More resources
EndNote: Download