Abstract.
When atrial tissue contracts, mechanically induced potentials (MIPs) are generated in fibroblasts, presumably by activation of a non-selective cation conductance G ns. Non-stimulated atrial fibroblasts had a mean (±SD) membrane potential (E m) of –22±2 mV and an input resistance of 510±10 MΩ. MIP amplitude (A MIP) was 38±4 mV when current injection had polarised E m to V m=–50 mV. The slope of the function relating A MIP to V m can be regarded as a mechanosensitive factor (X ms) that describes the relative increase in G ns during a MIP. Putative involvement of cytoskeletal fibres in activation of G ns was studied by delivering drugs from the intracellular recording microelectrode. Destabilisation of F-actin by 0.2 mM cytochalasin D reduced A MIP from 38 to 16 mV and X ms from 5 to 1.8. Destabilisation of tubulin with 0.2 mM colchicine reduced A MIP to 21 mV and X ms to 2.1. The combination colchicine plus cytochalasin D reduced A MIP to 9 mV and X ms to 1.4. Promoting F-actin stability with exogenous adenosine 5′-triphosphate (ATP) increased A MIP and X ms and attenuated the effects of cytochalasin D. Similarly, facilitation of tubulin stability with guanosine 5′-triphosphate (GTP) or taxol increased A MIP and X ms and attenuated the effects of colchicine. The results suggest that transfer of mechanical energy from the deformed fibroblast surface to the G ns channel protein depends on intact F-actin and tubulin fibres.
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Received after revision: 27 February 2001
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Kamkin, .A., Kiseleva, .I., Wagner, .K. et al. Mechanically induced potentials in rat atrial fibroblasts depend on actin and tubulin polymerisation. Pflügers Arch - Eur J Physiol 442, 487–497 (2001). https://doi.org/10.1007/s004240100564
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DOI: https://doi.org/10.1007/s004240100564