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Department of Physiology and Biophysics, State University of New York, Buffalo, New York 14214
Mechanoelectric
transduction can initiate cardiac arrhythmias. To examine the origins
of this effect at the cellular level, we made whole cell voltage-clamp
recordings from acutely isolated rat ventricular myocytes under
controlled strain. Longitudinal stretch elicited noninactivating inward
cationic currents that increased the action potential duration. These
stretch-activated currents could be blocked by 100 µM
Gd3+ but not by octanol. The current-voltage relationship
was nearly linear, with a reversal potential of approximately 
6
mV in normal Tyrode solution. Current density varied with sarcomere
length (SL) according to I (pA/pF) = 8.3 5.0SL (µm). Repeated attempts to record single
channel currents from stretch-activated ion channels failed, in accord
with the absence of such data from the literature. The inability to
record single channel currents may be a result of channels being
located on internal membranes such as the T tubules or, possibly,
inactivation of the channels by the mechanics of patch formation.
ion channel; patch clamp; mechanical stress; simulation; sarcomere
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