Excess plasma volume is a significant contributor to the hypertensive state. Atrial volume receptors (AVR) are an integral part of the neural circuitry that maintains plasma volume homeostasis. Abnormal mechano-sensing or transduction altered inadvertently by drug therapy may contribute to cardiovascular disease such as hypertension and heart failure. However, the molecular basis for mechano transduction in AVRs has not been studied. This study aims to characterize cardiac vagal AVRs by first developing a reliable preparation using an isolated innervated rat atrium. Single cardiac vagal sensory recordings were obtained whilst recording atrial contractile state. A neuroanatomical and functional study has commenced to determine which ion channels are expressed and required for action potential generation during physiological stimulation of these receptors. Wistar rats (145±20g; n=3) were euthanised with a stunning blow to the head followed swiftly by cervical dislocation. The intact right atrium was immediately harvested and superfused with oxygenated (95% O2, 5% CO2) Krebs solution at room temperature. All branches of the right vagus were dissected away with the exception of the cardiac branch. Right atrial contractile force was recorded via a force transducer. Using a suction electrode, the thoracic vagus was probed for action potentials generated as a result of AVR mechanotransduction, as determined by probing the atrial wall with Von Frey filaments (1.6mN). Thus far the recordings have yielded units with long refractory periods (15±4.58ms) as determined by interval time histograms. Cardiac triggered post stimulus time histograms showed that most action potential firing was not coupled with atrial contraction. Data is presented as Mean ± S.E.M. Proteins expressed in AVRs could provide novel drug targets for the regulation of cardiovascular homeostasis (1). Early experiments showed that introduction of the TRPV4 channel antagonist Ruthenium Red (50µM) inhibited action potential generation in response to mechanical probing via Von Frey filaments. Knowledge of the mechanism whereby the mechanical perturbation is transduced into a neural input to the brain will lead to a better understanding of how they contribute to normal cardiovascular control. It is anticipated that this novel preparation will contribute to understanding the physiology of AVRs. ​All procedures described conform with the Health Products Regulatory Authority of Ireland and Physiological Society ethical requirements.