Mechanoelectric transduction can initiate cardiac arrhythmias. To examine t
he origins of this effect at the cellular level, we made whole cell voltage
-clamp recordings from acutely isolated rat ventricular myocytes under cont
rolled strain. Longitudinal stretch elicited noninactivating inward cationi
c currents that increased the action potential duration. These stretch-acti
vated currents could be blocked by 100 mu M Gd3+ but not by octanol. The cu
rrent-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 (mu m). Repeated
attempts to record single channel currents from stretch-activated ion chan
nels failed, in accord with the absence of such data from the literature. T
he inability to record single channel currents may be a result of channels
being located on internal membranes such as the T tubules or, possibly, ina
ctivation of the channels by the mechanics of patch formation.