The study identifies stretch-activated ion channels in ventricular myocytes, suggesting a cellular mechanism where beat-to-beat tension or osmotic balance modulates membrane conductance.
Patch-clamp recordings from ventricular myocytes of neonatal rats identified ionic channels that open in response to membrane stretch caused by negative pressures (1 to 6 cm Hg) in the electrode. The stretch response, consisting of markedly increased channel opening frequency, was maintained, with some variability, during long (greater than 40 seconds) stretch applications. The channels have a conductance averaging 120pS in isotonic KCl, have a mean reversal potential 31 mV depolarized from resting membrane potential, and do not require external Ca++ for activation. The channels appear to be relatively non-selective for cations. Since they are gated by physiological levels of tension, stretch-activated channels may represent a cellular control system wherein beat-to-beat tension and/or osmotic balance modulate a portion of membrane conductance.
Craelius et al. (1988) studied this question.