Hypertension is a major risk factor for stroke and heart failure, and is also a leading cause of chronic kidney failure. To maintain an appropriate cardiac output the central nervous system (CNS) requires information from the periphery regarding blood pressure and volume. Sensors detect changes in these parameters and signal to the CNS where the information is integrated so that the brain can regulate efferent sympathetic activity to maintain cardiovascular homeostasis. Atrial volume receptors (AVRs) are specialised nerve endings found in the atrial wall and the entrances of the major blood vessels [1]. They detect the change in volume as blood returns to the heart. The literature provides classic descriptions of the electrical output from these receptors [2,3], however knowledge of their morphology is limited and they still await molecular characterisation. We have shown previously that members of the epithelial sodium channel (ENaC)/Degenerin /acid sensing ion channel (ASIC) family are major contributors to mechanotransduction in rat muscle spindles [4]. Transient receptor potential (TRP) proteins have also been implicated in mechanosensation in heart as well as other tissues [5]. Three male Hooded Lister rats were killed according to Schedule 1 of the Animals (Scientific Procedures) Act 1986. The atria were removed and fixed in 4% formaldehyde at 4oC. Following cryoprotection in sucrose/phosphate buffered saline (PBS), venoatrial regions were dissected, frozen and 16µm cryosections collected. Labelling was carried out with a range of anti-channel antibodies (ASIC2, ASIC3, ENaCα, ENaCβ, ENaCγ, TRPC1, TRPC4/5, TRPC6, TRPV4) together with either anti-synaptophysin (SYN) as a vesicle marker or anti-neurofilament (NF) antibodies to identify nerves. For controls anti-channel antibodies were omitted. Following washing in PBS, secondary antibodies (AF 594 + AF 488) were applied for one hour. The slides were washed in PBS and mounted in PBS/glycerol. Slides were viewed under a Zeiss Fluorescent microscope. TRPC1-like immunoreactivity (IR) was observed in ganglion cells and nerves of the epicardium; and also in sensory endings of the endocardium, where it was coincident with both SYN-IR and NF-IR. Strong TRPV4-like IR was likewise seen in nerves and ganglion cells. It was coincident with SYN-IR in all three layers of the heart wall. Immunoreactivity 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. Elucidation of the process whereby changes in returning blood volume are detected and signalled to the CNS is necessary to inform our understanding of how normal cardiovascular homeostasis malfunctions in disease. This will require a comprehensive knowledge of the proteins involved.