POSSIBLE STIMULATION OF NA-K+-ATPASE BY NO PRODUCED FROM SODIUM-NITRITE BY ULTRAVIOLET-LIGHT IN MOUSE GASTRIC FUNDAL STRIP()

Citation
N. Yaktubay et al., POSSIBLE STIMULATION OF NA-K+-ATPASE BY NO PRODUCED FROM SODIUM-NITRITE BY ULTRAVIOLET-LIGHT IN MOUSE GASTRIC FUNDAL STRIP(), General pharmacology, 32(1), 1999, pp. 159-162
Citations number
25
Categorie Soggetti
Pharmacology & Pharmacy
Journal title
ISSN journal
03063623
Volume
32
Issue
1
Year of publication
1999
Pages
159 - 162
Database
ISI
SICI code
0306-3623(1999)32:1<159:PSONBN>2.0.ZU;2-1
Abstract
1. In the present study, we investigated the roles of Na+-K+-ATPase an d extracellular Na+ or Ca2+ ions in ultraviolet (UV) light-induced pho torelaxation of methacholine contracted mouse isolated gastric fundus in the presence of NaNO2 (50 mu M) 2. Ouabain (1-500 mu M), sodium van adate (10 mu M to 3 mM) and amiloride (1-100 mu M) completely inhibite d the photorelaxation in a concentration dependent manner. 3. Metaboli c inhibitors, sodium azide (10-100 mu M), 2,4-dinitrophenol (100 mu M to 1 mM) and sodium fluoride (100 mu M to 1 mM) significantly reduced photorelaxation. 4. Substitution of sucrose, lithium or KCl with extra cellular Na+ completely abolished the photorelaxant responses. 5. Repl acement of all extracellular CaCl2 with BaCl2 also completely inhibite d UV-induced relaxation. 6. Verapamil (1-10 mu M) decreased UV-induced relaxation significantly. 7. These results suggest that nitric oxide produced from NaNO2 by UV-light in mouse gastric fundus probably stimu lates Na+-K+-ATPase activity, and photorelaxation of gastric smooth mu scle is dependent on extracellular Na+ and Ca2+ ions. (C) 1998 Elsevie r Science Inc.