Vanadium-induced Cl(-)-secretion in rabbit descending colon is mediated by prostaglandins.
Vanadium in the 4+ (vanadyl-ion) and 5+ (vanadate-ion) oxidation state stimulates furosemide-sensitive electrogenic Cl- secretion in isolated epithelia of rabbit descending colon. This effect is associated with an increased release of prostaglandin E2 from the tissue. Inhibitors of phospholipase A2 or cyclooxygenase abolish both vanadium-induced release of prostaglandin E2 and Cl- secretion. Neuronal mechanisms are not likely to be involved, as tetrodotoxin does not affect the vanadate induced Cl- secretion. Although vanadate is known to inhibit Na+,K(+)-ATPase activity, no inhibition of active Na+ transport was observed in intact colonic epithelia suggesting a rapid intracellular reduction of vanadate ions to vanadyl ions which have no inhibitory effect on the Na+,K(+)-ATPase. The present findings therefore indicate that vanadate stimulated colonic Cl- secretion involves intracellular conversion of vanadate to vanadyl and release of prostaglandin E2.
Plass
H
H
Pharmakologisches Institut, Universität Wien, Vienna, Austria.
Roden
M
M
Wiener
H
H
Turnheim
K
K
D000818:Animals; D002712:Chlorides / Q000378:metabolism*; D003106:Colon / Q000378:metabolism*; D015232:Dinoprostone / Q000502:physiology*; D005665:Furosemide / Q000494:pharmacology; D066298:In Vitro Techniques; D007700:Kinetics; D011817:Rabbits; D013779:Tetrodotoxin / Q000494:pharmacology; D014639:Vanadium / Q000494:pharmacology*
D002712:Chlorides; D014639:Vanadium; D013779:Tetrodotoxin; D005665:Furosemide; D015232:Dinoprostone