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      Mechanically activated currents in chick heart cells.

      The Journal of Membrane Biology
      Action Potentials, Animals, Calcium, pharmacology, Chick Embryo, Chlorides, Gadolinium, Heart, drug effects, embryology, physiology, Heart Rate, Hypotonic Solutions, Ion Channel Gating, Ion Channels, Neurotoxins, Patch-Clamp Techniques, Peptides, Cyclic, Potassium, Pressure, Sodium, Spider Venoms

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          Abstract

          As predicted from stretch-induced changes of rate and rhythm in the heart, acutely isolated embryonic chick heart cells exhibit whole-cell mechanosensitive currents. These currents were evoked by pressing on cells with a fire polished micropipette and measured through a perforated patch using a second pipette. The currents were carried by Na+ and K+ but not Cl-, and were independent of external Ca2+. The currents had linear I/V curves reversing at -16 mV and were completely blocked by Gd3+ >/= 30 microM and Grammostola spatulata venom at a dilution of 1:1000. Approximately 20% of cells showed time dependent inactivation. In contrast to direct mechanical stimulation, hypotonic volume stress produced an increase in conductance for anions rather than cations-the two stimuli are not equivalent. The cells had two types of stretch-activated ion channels (SACs): a 21 pS nonspecific cation-selective reversing at -2 mV and a 90 pS K+ selective reversing at -70 mV in normal saline. The activity of SACs was strongly correlated with the presence of whole-cell currents. Both the whole-cell currents and SACs were blocked by Gd3+ and by Grammostola spatulata spider venom. Mechanical stimulation of spontaneously active cells increased the beating rate and this effect was blocked by Gd3+. We conclude that physiologically active mechanosensitive currents arise from stretch activated ion channels.

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