Indirect evidence that anoxia exposure and cold acclimation alter transarcolemmal Ca2+ flux in the cardiac pacemaker, right atrium and ventricle of the red-eared slider turtle (Trachemys scripta).

We indirectly assessed if altered transarcolemmal Ca2+ flux accompanies the decreased cardiac activity displayed by Trachemys scripta with anoxia exposure and cold acclimation. Turtles were first acclimated to 21 °C or 5 °C and held under normoxic (21N; 5N) or anoxic conditions (21A; 5A). We then compared the response of intrinsic heart rate (fH) and maximal developed force of spontaneously contracting right atria (Fmax,RA), and maximal developed force of isometrically-contracting ventricular strips (Fmax,V), to Ni2+ (0.1-10 mM), which respectively blocks T-type Ca2+ channels, L-type Ca2+ channels and the Na+-Ca2+-exchanger at the low, intermediate and high concentrations employed. Dose-response curves were established in simulated in vivo normoxic (Sim Norm) or simulated in vivo anoxic extracellular conditions (Sim Anx; 21A and 5A preparations). Ni2+ decreased intrinsic fH, Fmax,RA and Fmax,V of 21N tissues in a concentration-dependent manner, but the responses were blunted in 21A tissues in Sim Norm. Similarly, dose-response curves for Fmax,RA and Fmax,V of 5N tissues were right-shifted, whereas anoxia exposure at 5 °C did not further alter the responses. The influence of Sim Anx was acclimation temperature-, cardiac chamber- and contractile parameter-dependent. Combined, the findings suggest that: (1) reduced transarcolemmal Ca2+ flux in the cardiac pacemaker is a potential mechanism underlying the slowed intrinsic fH of anoxic turtles at 21 °C, but not 5 °C, (2) a downregulation of transarcolemmal Ca2+ flux may aid cardiac anoxia survival at 21 °C and prime the turtle myocardium for winter anoxia and (3) confirm that altered extracellular conditions with anoxia exposure can modify turtle cardiac transarcolemmal Ca2+ flux.