The Alaska blackfish () remains active at cold temperatures when experiencing aquatic hypoxia without air access. To discern the cardiophysiological adjustments that permit this behaviour, we quantified the effect of acclimation from 15°C to 5°C in normoxia (15N and 5N fish), as well as chronic hypoxic submergence (6-8 weeks; ∼6.3-8.4 kPa; no air access) at 5°C (5H fish), on and spontaneous heart rate (), electrocardiogram, ventricular action potential (AP) shape and duration (APD), the background inward rectifier () and rapid delayed rectifier () K currents and ventricular gene expression of proteins involved in excitation-contraction coupling. was ∼50% slower in 5N than in 15N fish, but 5H fish did not display hypoxic bradycardia. Atypically, cold acclimation in normoxia did not induce shortening of APD or alter resting membrane potential. Rather, QT interval and APD were ∼2.6-fold longer in 5N than in 15N fish because outward and were not upregulated in 5N fish. By contrast, chronic hypoxic submergence elicited a shortening of QT interval and APD, driven by an upregulation of The altered electrophysiology of 5H fish was accompanied by increased gene expression of (3.5-fold; K11.2 of ), (7.4-fold; K2.2 of ) and (2.9-fold; K2.4 of ). 5H fish also exhibited a unique gene expression pattern that suggests modification of ventricular Ca cycling. Overall, the findings reveal that Alaska blackfish exposed to chronic hypoxic submergence prioritize the continuation of cardiac performance to support an active lifestyle over reducing cardiac ATP demand.
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http://dx.doi.org/10.1242/jeb.225730 | DOI Listing |
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Department of Ophthalmology, The Second Hospital &Clinical Medical School, Lanzhou University, Gansu 730000, China. Electronic address:
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Department of Nephrology, Affiliated Hospital of Xuzhou Medical University, 221002, China.
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School of Integrated Chinese Medicine and Western Medicine, Anhui University of Chinese Medicine Hefei 230012, China Anhui Province Key Laboratory of Chinese Medicinal Formula Hefei 230012, China.
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View Article and Find Full Text PDFChronic exposure to high altitudes causes pathophysiological cardiac changes that are characterized by cardiac dysfunction, cardiac hypertrophy, and decreased energy reserves. However, finding specific pharmacological interventions for these pathophysiological changes is challenging. In this study, we identified tetramethylpyrazine (TMP) as a promising drug candidate for cardiac dysfunction caused by simulated high-altitude exposure.
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