The role of intracellular Ca2+ under hypercapnic acidosis of cardiac muscle: Comparative aspects

Abstract

1. Under hypercapnic acidosis an initial decrease of myocardial contractile force is seen, but in some vertebrate species it is followed by a recovery. The resulting force level is higher in air-breathers, like a turtle (Pseudemys scripta), a snake (Vipera berus), and the laboratory rat, than in the waterbreathing fishes, trout and carp. The hearts of the leopard frog and grass frog are intermediate although the former tolerate hypercapnic acidosis better than the latter. 2. Cyanide does not affect the hypercapnic force development of the leopard frog, while it induces a recovery process in that of the grass frog. Since cyanide is known to release intracellularly bound Ca2+ this suggests that the recovery involves a changed Ca2+ distribution. 3. Incubation of cardiac strips fromVipera berus and trout in a Na+- and Ca2+-free Ringer causes an increase in resting tension. Under hypercapnic acidosis a decrease of this tension occurs which, however, for the strips from the viper is followed by recovery. The recovery process thus seems to be independent of extracellular Ca2+ or Na+. It also seems independent of the Ca2+ contained in the sarcoplasmatic reticulum, since the recovery of resting tension in the viper strips is unaffected by pretreatment with caffeine. 4. In viper myocardial strips, which develop high force under anoxia, the force loss by acidosis is increased and spontaneous recovery substantially depressed when hypercapnia is imposed after a 60 min pretreatment with agents unloading mitochondrial Ca2+-stores (anoxia and anoxia + oligomycin). 5. These findings favour the hypothesis that hypercapnic acidosis triggers the release of Ca2+ from intracellular stores, probably from mitochondria.