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Myocardial TRPV activation associated with high fat diet and cardioprotection
Author(s) -
Haar Lauren Lynn,
Rubinstein Jack,
Tranter Michael,
Jiang Min,
Jones W Keith
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.573.14
Subject(s) - trpv , cardioprotection , transient receptor potential channel , trpv1 , medicine , myocardial infarction , endocrinology , cardiac function curve , chemistry , pharmacology , heart failure , receptor
Clinical data suggests obese patients have improved outcomes after myocardial infarction as compared to non‐obese patients. It has been shown that cardioprotective effects of high fat diet are dependent upon transient receptor potential vanilloid 1 (TRPV1) channel activation. However, there are six TRPV channels and, to date, little is known about the expression or function of TRPV 2–6 in the heart. The goal of this study was to investigate the expression of the six TRPV channels in the myocardium and to evaluate their potential role in the link between obesity/high fat diet and cardioprotection. Our results show expression of all six TRPV genes in the myocardium. In addition, mice subjected to ischemic stimuli or maintained on a high fat diet display increases in TRPV channel expression. We hypothesize that TRPV channel activation by high fat diet plays a role in modulating myocardial function and cell survival. To understand the role of TRPV channels in the myocardium, we utilized echocardiography and examined the effect of TRPV channel activation, using relatively selective pharmacological agents, on in vivo cardiac function. We also investigated the expression and effect of TRPV channel activation on the function of isolated cardiomyocytes. TRPV channels play an important role in regulating cardiac function and may represent potential therapeutic targets for the treatment of cardiac pathologies. This work was supported by NIH grant R01 HL63034 (WKJ).