Cardiovascular actions of nickel ions.
The effects of Ni2+ on contractility, NADH-fluorescence, O2-consumption and total coronary resistance (TCR) of isolated perfused rat heart were studied in the presence of glucose or pyruvate and at different perfusate calcium concentations (Cap2+). Ni2+ 1 mM, abolished contractility, reduced O2-consumption, increased TCR and caused biphasic NADH-fluorescenceresponse, i.e., an initial reduction followed by NADH oxidation, regardless of the substrate present. Three-fold elevation of Cap2+, from 1.3 to 3.9 mM restored contractility and O2-consumption while enhancing the increase of TCR. NADH-oxidation was antagonized by excess Cap2+ in the presence of glucose only. Inhibition of cardiac contractility in response to increasing concentrations of N2+ (10(-7)--10(-3) M), in the presence of 1.3 mM  Cap2+, proved to be dose-dependent, whereas the amplitude of TCR elevation reached its maximum already at Ni2+ concentration of 10(-6) M. The present results emphasize the biomedical significance of this trace metal.
D000818:Animals; D002118:Calcium / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D066298:In Vitro Techniques; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism; D009243:NAD / Q000378:metabolism; D009532:Nickel / Q000494:pharmacology*; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D014655:Vascular Resistance / Q000187:drug effects
D009243:NAD; D009532:Nickel; D002118:Calcium