Effect of Ni2+, Co2+, Zn2+, Fe2+, Cd2+, Hg2+, Cu2+ and VO-3 on coronary vascular resistance in the isolated perfused rat heart.
The coronary vascular effect of various divalent cations and of sodium-metavanadate was compared in isolated perfused rat hearts. Their order of activity was as follows (the concentrations (microM) evoking a half-maximum increase of coronary resistance are indicated (in parentheses): Ni2+ (0.03) greater than Co2+ (0.1) greater than Hg2+ (0.16) greater than VO-3 (0.2) greater than Cu2+ (15) greater than Zn (50). Iron (Fe2+) and cadmium (Cd2+) were ineffective. The order of coronary vasoconstrictor potency of these metal ions differs from the order of their other physico-chemical properties indicating that their coronary action cannot be explained as being singly a consequence of ion-membrane interaction. In contrast to Ni2+, the effect of Hg2+ was totally inhibited by phenoxybenzamine (10(-5)M) indicating that coronary vasoconstriction induced by mercury ions is mediated by alpha-receptors. Coronary vasoconstriction induced by sodium-meta-vanadate was resistant to verapamil while removal of external Ca2+ potentiated its effect. These data suggest that in contrast to Ni2+ and Hg2+, vanadate increases coronary resistance by mobilizing intracellular Ca2+ in vascular smooth muscle cells.
D000818:Animals; D002413:Cations, Divalent; D003035:Cobalt / Q000494:pharmacology; D003300:Copper / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects*; D005260:Female; D008297:Male; D008628:Mercury / Q000494:pharmacology; D009532:Nickel / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D014639:Vanadium / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects*; D014700:Verapamil / Q000494:pharmacology; D015032:Zinc / Q000494:pharmacology
D002413:Cations, Divalent; D014639:Vanadium; D003035:Cobalt; D003300:Copper; D009532:Nickel; D014700:Verapamil; D008628:Mercury; D015032:Zinc