Subchronic treatment with vanadate does not potentiate the toxicity of cardiac glycosides.
Since it has been claimed that vanadate is an endogenous regulator of Na/K-ATPase activity and that it potentiates the toxicity of cardiac glycosides, we were alarmed to discover that certain Finnish physicians were prescribing vanadate in combination with other trace minerals to elderly patients for many different chronic diseases (e.g., cancer, rheumatism). To study the interaction of vanadate and cardiac glycosides, we fed vanadate in the drinking water (25 micrograms/mL) to guinea pigs for 20 d, and studied either their sensitivity to the acute toxicity of the cardiac glycoside ouabain or whether the vanadate would influence the subacute toxicity of ouabain. Vanadate had no influence on the toxicity of ouabain either acute or subchronically administered, nor was there any sign of inhibition of Na/K-ATPase activity as measured by 86Rb-uptake into intact erythrocytes (RBCs), RBC content of sodium or potassium or Na/K-ATPase activity in RBC membranes prepared from the vanadate-treated guinea pigs. Vanadate had been absorbed in substantial quantities from the gastrointestinal tract, since serum, heart, liver, and especially kidney contained measurable amounts of vanadium in contrast to controls, but it is concluded that this vanadate is not in a biologically active form.
MacDonald
E
E
Department of Pharmacology University of Kuopio, Finland.
Lihtamo
H
H
Hellevuo
K
K
Komulainen
H
H
D000818:Animals; D004357:Drug Synergism; D004562:Electrocardiography / Q000187:drug effects; D004912:Erythrocytes / Q000201:enzymology; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D008297:Male; D010042:Ouabain / Q000633:toxicity*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D014018:Tissue Distribution; D014638:Vanadates / Q000493:pharmacokinetics / Q000494:pharmacology*
D014638:Vanadates; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase