Neurogenic hypothesis of cardiac ischemic pain

Wang, Yan; Zeng, Xiaolin; Gao, Ranran; Wang, Xiumin; Wang, Xiaotong; 鄭, 国慶

doi:10.1016/j.mehy.2008.12.001

Cited by 4 publications

(1 citation statement)

References 19 publications

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“…6 This efferent function of nociceptors is known as neurogenic inflammation, which would result in vessel dilatation and increase vessel permeability as was observed in skin and muscle and recently proposed in the heart. 23, 24 Because ASIC3 is predominately expressed in peptidergic sensory neurons, 25-27 ASIC3-expressing cardiac afferents may release neuropeptides in response to myocardial ischemia and thus increase blood flow in the coronary artery and shorten the periods of …”

Section: Discussionmentioning

confidence: 99%

Acid-Sensing Ion Channel 3, But Not Capsaicin Receptor TRPV1, Plays a Protective Role in Isoproterenol-Induced Myocardial Ischemia in Mice

Cheng

Chen

Cheng

et al. 2011

Circ J

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Background: Cardiac 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 myocardial ischemia. However, studies comparing the physiological roles of ASIC3 and TRPV1 in the neuronal - cardiac sensing circuits in vivo are lacking. Methods and Results:Isoproterenol (1.5 mg/kg, intraperitoneally) was used to induce transient myocardial ischemia in Asic3 +/+ and Asic3 -/-mice and a radio-telemetry system was used for electrocardiography with mice in a conscious state. Isoproterenol-induced myocardial 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.Conclusions: An isoproterenol-induced myocardial ischemia model mimicking clinical conditions of early cardiac angina was used to demonstrate that ASIC3 but not TRPV1 plays a protective role in sensing myocardial ischemia. (Circ J 2011; 75: 174 - 178)

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Section: Discussionmentioning

confidence: 99%