PMID- 11510879
OWN - NLM
STAT- MEDLINE
DCOM- 20020125
LR  - 20190726
IS  - 0031-6768 (Print)
IS  - 0031-6768 (Linking)
VI  - 442
IP  - 4
DP  - 2001 Jul
TI  - Mechanically induced potentials in rat atrial fibroblasts depend on actin and 
      tubulin polymerisation.
PG  - 487-97
AB  - 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.
FAU - Kamkin, A
AU  - Kamkin A
AD  - Department of Physiology, Martin-Luther-University Halle, Germany.
FAU - Kiseleva, I
AU  - Kiseleva I
FAU - Wagner, K D
AU  - Wagner KD
FAU - Scholz, H
AU  - Scholz H
FAU - Theres, H
AU  - Theres H
FAU - Kazanski, V
AU  - Kazanski V
FAU - Lozinsky, I
AU  - Lozinsky I
FAU - Gunther, J
AU  - Gunther J
FAU - Isenberg, G
AU  - Isenberg G
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Pflugers Arch
JT  - Pflugers Archiv : European journal of physiology
JID - 0154720
RN  - 0 (Actins)
RN  - 0 (Antineoplastic Agents, Phytogenic)
RN  - 0 (Nucleic Acid Synthesis Inhibitors)
RN  - 0 (Polymers)
RN  - 0 (Tubulin)
RN  - 22144-77-0 (Cytochalasin D)
RN  - 660YQ98I10 (Potassium Chloride)
RN  - 86-01-1 (Guanosine Triphosphate)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - P88XT4IS4D (Paclitaxel)
RN  - SML2Y3J35T (Colchicine)
SB  - IM
MH  - Actins/*metabolism
MH  - Adenosine Triphosphate/pharmacology
MH  - Animals
MH  - Antineoplastic Agents, Phytogenic/pharmacology
MH  - Colchicine/pharmacology
MH  - Cytochalasin D/pharmacology
MH  - Cytoskeleton/drug effects/metabolism
MH  - Electrophysiology
MH  - Fibroblasts/*physiology
MH  - Guanosine Triphosphate/pharmacology
MH  - Heart Atria/cytology
MH  - Male
MH  - Membrane Potentials/drug effects/physiology
MH  - Models, Biological
MH  - Myocardium/*cytology
MH  - Nucleic Acid Synthesis Inhibitors/pharmacology
MH  - Paclitaxel/pharmacology
MH  - Polymers/metabolism
MH  - Potassium Chloride
MH  - Rats
MH  - Rats, Wistar
MH  - Stress, Mechanical
MH  - Tubulin/*metabolism
EDAT- 2001/08/21 10:00
MHDA- 2002/01/26 10:01
CRDT- 2001/08/21 10:00
PHST- 2001/08/21 10:00 [pubmed]
PHST- 2002/01/26 10:01 [medline]
PHST- 2001/08/21 10:00 [entrez]
AID - 10.1007/s004240100564 [doi]
PST - ppublish
SO  - Pflugers Arch. 2001 Jul;442(4):487-97. doi: 10.1007/s004240100564.