Nickel induces vasoconstriction in the isolated canine coronary artery by a tonic Ca2+-activation mechanism.

Abstract

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.