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TRPC1 and TRPV4 are expressed in sensory endings found in regions of venoatrial endocardium where atrial volume receptors are located
Author(s) -
Shenton Fiona,
Banks Robert,
Pyner Susan
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.1056.5
Subject(s) - mechanosensation , trpv4 , transient receptor potential channel , endocardium , trpc1 , free nerve ending , microbiology and biotechnology , ion channel , chemistry , anatomy , neuroscience , medicine , biology , receptor
Atrial volume receptors (AVRs) detect mechanical deformation as blood returns to the heart. Members of both the ENaC/Degenerin /ASIC and the Transient Receptor Potential (TRP) channel protein families have been implicated in mechanosensation. We have carried out immunohistological investigations to discover potential mechanosensitive ion channels in sensory endings of venoatrial endocardium. Synaptic‐like vesicles, commonly described in mechanosensory endings, are thought to play a key role in regulating afferent output. Double labelling was carried out with a range of anti‐channel antibodies (ENaCβ, ENaCγ, TRPC1, TRPC4/5, TRPC6, TRPV4) together with either anti‐synaptophysin as a vesicle marker or anti‐neurofilament (NF) to identify nerves. TRPC1‐like immunoreactivity (IR) was observed in ganglion cells and nerves of the epicardium, in myocytes; and also in sensory endings of the endocardium, where it was coincident with both synaptopphysin and NF‐IR. Strong TRPV4‐like IR was likewise seen in nerves and ganglion cells. It was coincident with synaptophysin‐IR in both myocardium and epicardium, however it did not appear to stain myocytes themselves. IR was not detected with any of the other anti‐channel antibodies. TRPC1 and TRPV4 channels merit further investigation as potential contributors to mechanosensation in AVRs. Research supported by EPSRC