Sodium-calcium exchange in dog heart mitochondria: effects of ischemia and verapamil.
Na+ - Ca2+ exchange was studied in two preparations of dog heart mitochondria isolated from normal and ischemic muscle following occlusion of the circumflex (CFX) coronary artery with or without prior verapamil infusion. Na+ - Ca2+ exchange in mitochondria isolated using polytron homogenization showed sigmoidal kinetics with phosphate, whereas mitochondria isolated using gentle nagarse treatment showed hyperbolic kinetics and a Vmax 60% greater than the polytron preparation. Nagarse did not alter the sigmoidal kinetics or exchange velocities of the polytron mitochondria observed with phosphate. With acetate, both preparations exhibited hyperbolic kinetics, and the sodium required for half-maximum activity was increased. Verapamil inhibited Na+ - Ca2+ exchange in both preparations with phosphate, but not with acetate. Thirty or sixty minutes of acute ischemia following CFX occlusion produced significant epicardial surface S-T elevation in the ischemic area and a decrease in myocardial segment shortening. Na+ - Ca2+ exchange of both ischemic preparations was depressed, and the kinetics of the polytron preparation changed to hyperbolic. Pretreatment of the experimental animals with verapamil (0.3 mg/kg) before 60 min of ischemia protected the exchange rates in both preparations, and the sigmoidicity of the polytron mitochondria was retained.
D000818:Animals; D000838:Anions; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D004285:Dogs; D005260:Female; D007700:Kinetics; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D014700:Verapamil / Q000494:pharmacology*
D000838:Anions; D012964:Sodium; D014700:Verapamil; D002118:Calcium