Abstract. When atrial tissue contracts, mechanically induced potentials (MIPs) are generated in fibroblasts, presumably by activation of a non-selective cation conductance Gns. Non-stimulated atrial fibroblasts had a mean (SD) membrane potential (Em) of 222mV and an input resistance of 51010M. MIP amplitude (AMIP) was 384mV when current injection had polarised Em to Vm=50mV. The slope of the function relating AMIP to Vm can be regarded as a mechanosensitive factor (Xms) that describes the relative increase in Gns during a MIP. Putative involvement of cytoskeletal fibres in activation of Gns was studied by delivering drugs from the intracellular recording microelectrode. Destabilisation of F-actin by 0.2mM cytochalasin D reduced AMIP from 38 to 16mV and Xms from 5 to 1.8. Destabilisation of tubulin with 0.2mM colchicine reduced AMIP to 21mV and Xms to 2.1. The combination colchicine plus cytochalasin D reduced AMIP to 9mV and Xms to 1.4. Promoting F-actin stability with exogenous adenosine 5-triphosphate (ATP) increased AMIP and Xms and attenuated the effects of cytochalasin D. Similarly, facilitation of tubulin stability with guanosine 5-triphosphate (GTP) or taxol increased AMIP and Xms and attenuated the effects of colchicine. The results suggest that transfer of mechanical energy from the deformed fibroblast surface to the Gns channel protein depends on intact F-actin and tubulin fibres.