A characteristic of hypertension and cardiovascular disease is an over-activation of the sympathetic nervous system [1]. The aetiology underlying the development and maintenance of this excitation is still not fully understood. An aspect of the regulatory process that has largely been ignored is the key role played by the sensory input from cardiac mechanoreceptors in sustaining appropriate cardiac output. One component of this input is the atrial volume reflex arc, initiated by receptors at the venous atrial junction of the heart which respond to changes in blood volume. Although atrial volume receptors have been reported to be primarily within the endocardium [2], details of the receptor location and mode of function have not been previously described. We have shown that Transient Receptor Potential (TRP) channels TRPC1 and TRPV4 are expressed within the endocardial layer of this region [3] and are therefore candidates as the mechanosensitive channel(s) which respond to mechanical deformations of the atrial wall. TRP proteins are nonselective cation channels, most of which allow the passage of Ca2+, the output from other stretch sensitive endings has been shown to be Ca2+ dependent [4] and small conductance Ca2+-activated K+ (SK) channels influence excitability in these endings [5]. We have used immunolabelling to test for the presence of the SK1-4 isoforms in this region. Three male Hooded Lister rats were killed under Schedule 1 of the Animals (Scientific Procedures) Act 1986. The atria, including entrances of the major vessels, were removed and fixed overnight in 4% formaldehyde. Following cryoprotection in sucrose/PBS, venous atrial regions were dissected out, frozen and 16µm cryosections collected. Double labelling was carried out with anti-SK antibodies together with the sensory nerve ending vesicle marker anti-synaptophysin (SYN). Appropriate secondary antibodies were applied to distinguish between anti-SK reactivity and the anti-SYN marker. Slides were viewed using a Zeiss Fluorescent microscope. Strong SK2-immunoreactivity (IR) was evident in nerve fibres within the epicardium. SK2-IR did not coincide with SYN-IR in this layer. SK2-IR was occasionally present within the myocardium and endocardium and here it did coincide with SYN-IR. SK4-IR was found in the endocardium giving small patches of diffuse labelling which appeared to be over epithelial cells, but did not coincide with SYN-IR. No evidence of SK1 or SK3 IR was found throughout this region. Since there was very little SK2 in the endocardium itself, and the SK4 expressed in this layer did not coincide with SYN-IR, these channels are unlikely to directly regulate afferent sensitivity in this instance. Nevertheless, their presence in this general area suggests they could influence responses to atrial stretch by other mechanisms.