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
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.