title: Mechanically induced potentials in rat atrial fibroblasts depend on actin and tubulin polymerisation.
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 -22 +/- 2 mV and an input resistance of 510 +/- 10 MS. MIP amplitude (AMIP) was 38+/-4 mV when current injection had polarised Em to Vm = -50 mV. 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 0.2 mM cytochalasin D reduced AMIP from 38 to 16 mV and Xms from 5 to 1.8. Destabilisation of tubulin with 0.2 mM colchicine reduced AMIP to 21 mV and Xms to 2.1. The combination colchicine plus cytochalasin D reduced AMIP to 9 mV 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.
authors.affiliation: Department of Physiology, Martin-Luther-University Halle, Germany.
authors.forename: A
authors.initials: A
authors.lastname: Kamkin
authors.forename: I
authors.initials: I
authors.lastname: Kiseleva
authors.forename: K D
authors.initials: KD
authors.lastname: Wagner
authors.forename: H
authors.initials: H
authors.lastname: Scholz
authors.forename: H
authors.initials: H
authors.lastname: Theres
authors.forename: V
authors.initials: V
authors.lastname: Kazanski
authors.forename: I
authors.initials: I
authors.lastname: Lozinsky
authors.forename: J
authors.initials: J
authors.lastname: Günther
authors.forename: G
authors.initials: G
authors.lastname: Isenberg
mesh_terms: D000199:Actins / Q000378:metabolism*; D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D000972:Antineoplastic Agents, Phytogenic / Q000494:pharmacology; D003078:Colchicine / Q000494:pharmacology; D015638:Cytochalasin D / Q000494:pharmacology; D003599:Cytoskeleton / Q000187:drug effects / Q000378:metabolism; D004594:Electrophysiology; D005347:Fibroblasts / Q000502:physiology*; D006160:Guanosine Triphosphate / Q000494:pharmacology; D006325:Heart Atria / Q000166:cytology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008954:Models, Biological; D009206:Myocardium / Q000166:cytology*; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D017239:Paclitaxel / Q000494:pharmacology; D011108:Polymers / Q000378:metabolism; D011189:Potassium Chloride; D051381:Rats; D017208:Rats, Wistar; D013314:Stress, Mechanical; D014404:Tubulin / Q000378:metabolism*
chemical_list: D000199:Actins; D000972:Antineoplastic Agents, Phytogenic; D019384:Nucleic Acid Synthesis Inhibitors; D011108:Polymers; D014404:Tubulin; D015638:Cytochalasin D; D011189:Potassium Chloride; D006160:Guanosine Triphosphate; D000255:Adenosine Triphosphate; D017239:Paclitaxel; D003078:Colchicine