• Ching-Feng Cheng, I-Lun Chen, Mei-Hsin Cheng, Wei-Shiung Lian, Chao-Chieh Lin, Terry B J Kuo, and Chih-Cheng Chen.
• Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan.
• Circ. J. 2011 Jan 1; 75 (1): 174-8.

BackgroundCardiac angina is the hallmark of myocardial ischemia, but the role of the cardiac sensory nerve has received relatively little attention. Recently, both acid-sensing ion channel 3 (ASIC3) and capsaicin receptor (TRPV1) have been suggested as important mediators in sensing cardiac ischemia. However, studies comparing the physiological roles of ASIC3 and TRPV1 in the neuronal-cardiac sensing circuits in vivo are lacking.Methods And ResultsIsoproterenol (1.5 mg/kg, intraperitoneally) was used to induce transient cardiac ischemia in Asic3(+/+) and Asic3(-/-) mice and a radio-telemetry system was used for electrocardiography with mice in a conscious state. Isoproterenol-induced cardiac ischemia was first demonstrated with ST-segment depression and further confirmed by hypoxia-mediated chemical reactions in cardiac tissue. Mice lacking Asic3 showed prolonged duration of ST-segment depression compared with Asic3(+/+) mice (44.3 ± 3.1 vs. 31.7 ± 2.9 min; P < 0.05). Although ischemia was transient, severe cardiac fibrosis was found in Asic3(-/-) but not in Asic3(+/+) mice littermates. In contrast, isoproterenol-injected Trpv1(+/+) and Trpv1(-/-) mice showed no difference in duration of ST-segment depression and, surprisingly, deletion of Trpv1 did not aggravate cardiac fibrosis.ConclusionsAn isoproterenol-induced cardiac ischemia model mimicking clinical conditions of early cardiac angina was used to demonstrate that ASIC3 but not TRPV1 plays a protective role in sensing cardiac ischemia.

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