Аннотация:We tested the hypothesis that both stretch‐activated channels (SACs) and intracellular calcium ([Ca 2+ ] i ) are important in the electrical response of single guinea‐pig ventricular myocytes to axial stretch. Myocytes were attached to carbon fibre transducers and stretched, sarcomere length increased by approximately 9 %, and there was a prolongation of the action potential duration. Streptomycin, a blocker of SACs, had no effect upon the shortening, [Ca 2+ ] i transients or action potentials of electrically stimulated, unstretched myocytes, at a concentration of 50 μ m , but at 40 μ m , prevented any stretch‐induced increase in action potential duration. Under action potential clamp, stretch elicited a current with a linear current‐voltage relationship that was inward at membrane potentials negative to its reversal potential of −30 mV, in 10 of 24 cells tested, and was consistent with the activation of non‐specific, cationic SACs. This current was not seen in any stretched cells that were exposed to 40 μ m streptomycin. However, exposure of cells to 5 μ m BAPTA‐AM, in order to reduce [Ca 2+ ] i transients, also abolished stretch‐induced prolongation of the action potential. We conclude that both SACs and [Ca 2+ ] i are important in the electrical response of cardiac myocytes to stretch, and propose that stretch‐induced changes in electrical activity and [Ca 2+ ] i may be linked by inter‐dependent mechanisms.
