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Reduced translocation of the TRPv1 receptor in afferent neurons of cardiomyopathic rats
Author(s) -
Nguyen Minh M,
Stout Laurence E,
Li Qinglu,
Garry Mary G
Publication year - 2012
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.26.1_supplement.1091.11
Subject(s) - trpv1 , chemistry , chromosomal translocation , medicine , cytoplasm , endocrinology , receptor , microbiology and biotechnology , cytosol , transient receptor potential channel , biology , biochemistry , gene , enzyme
Heart failure (HF) patients exhibit an abnormal exercise pressor reflex (EPR) in response to exercise. Previous studies have implicated the TrpV1 receptor, a vanilloid receptor and transmembrane ion channel, as a mediator of the EPR. A necessary step in activation of TRPv1 is translocation to the membrane. To determine if the translocation of TRPv1 is affected in HF, we compared the subcellular localization of TRPv1 in primary cultures of dorsal root ganglia (DRG) from normal and cardiomyopathic rats. DRGs (L4–L6) of normal or cardiomyopathic rats were evaluated in the presence or absence of NGF. Cells were stained for TrpV1 and fluorescence intensities of membrane and cytoplasm were quantified. Normal NGF treated DRG cells showed an increased ratio of membrane to cytoplasmic TrpV1 staining as compared to normal untreated control. In HF, the ratio of membrane to cytoplasmic TrpV1 was similar regardless of treatment. These results suggest that HF DRGs are impaired in their ability to recruit TrpV1 to the membrane. Furthermore, this suggests that abnormal EPR response in HF patients may be due, in part, to decreased TrpV1 activity due to reduced TrpV1 membrane localization. Studies supported by: NIH 2R01HL070242‐07A2 (MGG).