Department of Biological Sciences, University of Alaska Anchorage, Anchorage, AK 99508, United States of America.
Department of Biological Sciences, University of Alaska Anchorage, Anchorage, AK 99508, United States of America.
Comp Biochem Physiol A Mol Integr Physiol. 2021 Nov;261:111043. doi: 10.1016/j.cbpa.2021.111043. Epub 2021 Jul 29.
We indirectly assessed if altered transarcolemmal Ca 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 (f) and maximal developed force of spontaneously contracting right atria (F), and maximal developed force of isometrically-contracting ventricular strips (F), to Ni (0.1-10 mM), which respectively blocks T-type Ca channels, L-type Ca channels and the Na-Ca-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). Ni decreased intrinsic f, F and F of 21N tissues in a concentration-dependent manner, but the responses were blunted in 21A tissues in Sim Norm. Similarly, dose-response curves for F and F 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 Ca flux in the cardiac pacemaker is a potential mechanism underlying the slowed intrinsic f of anoxic turtles at 21 °C, but not 5 °C, (2) a downregulation of transarcolemmal Ca 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 Ca flux.
我们间接地评估了 Trachemys scripta 在缺氧暴露和冷适应下心脏活动降低时,跨细胞膜 Ca 流是否发生改变。首先将海龟适应于 21°C 或 5°C 并在常氧(21N;5N)或缺氧条件(21A;5A)下保存。然后,我们比较了内在心率(f)和自发性收缩右心房最大发展力(F)以及等长收缩心室条最大发展力(F)对 Ni(0.1-10mM)的反应,Ni 分别在低、中和高浓度下阻断 T 型 Ca 通道、L 型 Ca 通道和 Na-Ca 交换体。在模拟体内常氧(Sim Norm)或模拟体内缺氧细胞外条件(Sim Anx;21A 和 5A 制剂)下建立了剂量反应曲线。Ni 以浓度依赖性方式降低了 21N 组织的内在 f、F 和 F,但在 Sim Norm 中 21A 组织的反应变迟钝。同样,5N 组织的 F 和 F 的剂量反应曲线右移,而在 5°C 时缺氧暴露并未进一步改变反应。Sim Anx 的影响取决于适应温度、心脏腔室和收缩参数。综合来看,这些发现表明:(1)在 21°C 时缺氧海龟心脏起搏的跨细胞膜 Ca 流减少是固有 f 减慢的潜在机制,但在 5°C 时则不然,(2)跨细胞膜 Ca 流的下调可能有助于 21°C 时心脏的缺氧存活,并使海龟心肌为冬季缺氧做好准备,(3)证实缺氧暴露改变细胞外条件可以改变海龟心脏跨细胞膜 Ca 流。