Nickel induces vasoconstriction in the isolated canine coronary artery by a tonic Ca2+-activation mechanism.
Nickel chloride (NiCl2) at low concentration (1 microM) induced isometric force development in isolated canine coronary artery strips. The Ni2+-action was linearly dependent on extracellular Ca2+-concentration in the range of 0 to 5.0 mM. Verapamil (10(-6) - 10(-3) M) did not prevent or abolish Ni2+-induced coronary contraction, but nitroprusside sodium even at low concentration (10(-8) M) antagonized the tonic force development. The results indicate that the stimulation of force development by trace amounts of NiCl2 in isolated canine coronary artery strips is dependent on transmembrane Ca2+-influx which is mediated by the T-system of Ca2+-activation.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D004285:Dogs; D005260:Female; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology; D009532:Nickel / Q000494:pharmacology*; D009599:Nitroprusside / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects*; D014700:Verapamil / Q000494:pharmacology
D009599:Nitroprusside; C022838:nickel chloride; D009532:Nickel; D014700:Verapamil; D002118:Calcium