Dependence of nickel-induced coronary vasoconstriction on the activity of the electrogenic Na+, K+-pump.
The possible interactions between the vasoactive trace metal nickel ion (Ni2+) and membrane Na-K-ATPase in the isolated perfused rat heart and in the isolated canine coronary artery have been studied. The characteristic features of 1 microM Ni2+-induced contractile response in the canine coronary artery strip were similar to those evoked by the inhibition of Na-K-ATPase. Inhibition of the pump activity by ouabain (10(-4)M) or by K+-deficient Krebs solution prevented Ni2+-action both in the canine coronary artery strip and in the perfused rat heart, indicating that when Ni2+ causes coronary vasoconstriction the Na, K-exchange is influenced. Further studies are needed to clarify whether Ni2+ acts directly on the enzyme, or the vascular action of this trace metal depends on the ionic gradients maintained by the electrogenic Na-K-pump.
D000818:Animals; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D004285:Dogs; D005260:Female; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009532:Nickel / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D014655:Vascular Resistance / Q000187:drug effects; D014661:Vasoconstriction / Q000187:drug effects*
D007473:Ion Channels; D010042:Ouabain; C022838:nickel chloride; D009532:Nickel; D012964:Sodium; D011188:Potassium