Inhibition of the Na+-H+ exchanger with cariporide abolishes stretch-induced calcium but not sodium accumulation in mouse ventricular myocytes.

We address the question whether activation of the sodium-proton exchanger (NHE) does contribute to the stretch-induced accumulation of intracellular sodium and calcium in mouse ventricular myocytes. NHE-blocker cariporide (10 microM) were applied to the bath for 10 min. Axial stretch was applied for 2 min by increasing the distance between an adherent glass stylus and the patch pipette by 20%.

Increments in the concentrations of sodium and calcium in cell compartments of stretched mouse ventricular myocytes.

Increments in total intracellular sodium [Na] and calcium concentration [Ca], expected from stretch activation of non-selective cation current I(SAC), were quantified by means of electron probe microanalysis (EPMA) with 16 nm spatial resolution.Voltage-clamped mouse ventricular myocytes were stretched by increasing the distance between patch pipette and a cell-attached stylus by 20%. After 2 min stretch, cells were shock-frozen for EPMA.

Differential effects of stretch and compression on membrane currents and [Na+]c in ventricular myocytes.

Mechano-electrical feedback was studied in the single ventricular myocytes. A small fraction (approximately 10%) of the cell surface could be stretched or compressed by a glass stylus. Stretch depolarised, shortened the action potential and induced extra systoles.