The mechanism of large, excitation-dependent influx of 45Ca in the guinea-pig ventricular myocardium.
In the previous papers (Lewartowski et al. 1982; Pytkowski et al. 1983) we found that excitation-dependent uptake of 45Ca (EDU) ranges in the vascularly perfused guinea-pig ventricular myocardium from 40-359 mumol/kg of wet weight per single steady-state beat or post-rest beat. The present paper describes an attempt to find whether slow calcium channel or Na/Ca exchange provides the route of this large 45Ca influx. We found that EDU during steady-state stimulation (60/min) was completely blocked by both D-600 (1 mg/l) and Ni (2 mmol/l) whereas EDU in post-rest beats was blocked only by Ni. Low Na+ perfusion (50 mmol/l) increased transiently EDU in steady-state beats. This surplus EDU was not blocked by D-600 nor by Ni. Noradrenaline infused at the rate sufficient to increase contractile force by 50% at least doubled EDU both in the steady-state and in post-rest beats. It is proposed that Na/Ca exchange does not participate significantly to EDU under physiological conditions. The changes in this uptake evoked by the applied interventions could be expected if its route was provided by the slow Ca channel.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002132:Calcium Radioisotopes; D005711:Gallopamil / Q000494:pharmacology; D006168:Guinea Pigs; D006352:Heart Ventricles / Q000187:drug effects / Q000378:metabolism; D066298:In Vitro Techniques; D007700:Kinetics; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism*; D009532:Nickel / Q000494:pharmacology; D012964:Sodium / Q000494:pharmacology
D002132:Calcium Radioisotopes; D005711:Gallopamil; D009532:Nickel; D012964:Sodium; D002118:Calcium