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

• Published in: Cell calcium (Edinburgh) Vol. 34; no. 2; pp. 193 - 203
• Main Authors: Kondratev, Denis, Gallitelli, Maria Fiora
• Format: Journal Article
• Language: English
• Published: Netherlands 01.08.2003
• Subjects: Animals; Calcium - metabolism; Cell Compartmentation; Cell Nucleus - metabolism; Cytosol - metabolism; Electron Probe Microanalysis; Freezing; Heart Ventricles - cytology; Histone-Lysine N-Methyltransferase; In Vitro Techniques; Ion Channels - metabolism; Mice; Mitochondria - metabolism; Myocytes, Cardiac - metabolism; Nuclear Envelope - metabolism; Physical Stimulation; Protein Synthesis Inhibitors - pharmacology; Sodium - metabolism; Streptomycin - pharmacology
• ISSN: 0143-4160
• DOI: 10.1016/S0143-4160(03)00084-8

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. Stretch incremented [Na] in peripheral cytosol from 23 to 48 mM, central cytosol from 17 to 29 mM, central mitochondria from 10 to 21 mM, nuclear envelope from 43 to 71 mM, nucleus from 12 to 24 mM. Stretch increased total [Ca] in peripheral cytosol from 570 to 840 microM, central cytosol from 404 to 840 microM. Mitochondrial [Ca] did not change. Stretch increased [Ca] in both nucleus (from 180 to 300 microM) and nuclear envelope (from 933 to 1530 microM) suggesting a calcium barrier function for the envelope. Block of I(SAC) by 50 microM streptomycin abolished stretch-induced increments in [Na] suggesting Na(+) influx with I(SAC) as underlying mechanism. Streptomycin abolished the stretch-induced increase in peripheral but not in central cytosolic [Ca], as if additional mechanisms to I(SAC) were involved in elevating central [Ca].