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Am J Physiol Heart Circ Physiol 273: H1832-H1840, 1997;
0363-6135/97 $5.00
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Vol. 273, Issue 4, H1832-H1840, October 1997

Cytoskeleton modulates coupling between availability and activation of cardiac sodium channel

Victor A. Maltsev and Albertas I. Undrovinas

Division of Cardiovascular Medicine, Henry Ford Heart and Vascular Institute, Detroit, Michigan 48202-2689

The aim of this study was to investigate modulation of voltage-dependent steady-state activation and availability from inactivation of the cardiac Na+ channel by the cytoskeleton. As an experimental approach, we used long-lasting monitoring [63 ± 5 (SE) min] of the half-point potentials of the steady-state availability curve (V1/2A) and normalized conductance curve (V1/2G) in 116 rat ventricular cardiomyocytes by whole cell patch clamp at 22-24°C. Both half-point potentials shifted in the negative direction with time as an exponentially saturating change, with the shift of V1/2G being smaller and faster. An F-actin disrupter, cytochalasin D (Cyto-D, 20 µM), accelerated the rate of the V1/2A shift but decreased the range of the V1/2G shift. An F-actin stabilizer, phalloidin (100 µM), temporarily (for 28.2 ± 2.2 min, n = 15) prevented the V1/2A shift but did not influence the V1/2G shift. The best fit for the V1/2G-V1/2A relationship in untreated cells (1,021 data points measured in 51 cells) was a second-degree (2.06) power function. Cytoskeleton-directed agents modified the relationship. In Cyto-D-treated cells, the V1/2G-V1/2A relationship was shifted (by 2.5 mV) toward positive V1/2G. On the contrary, a microtubule stabilizer, taxol (100 µM), shifted the relationship toward negative V1/2G (by 12.2 mV). We conclude that coupling between availability and activation is modulated by F-actin-based and microtubular cytoskeleton.

sodium current; patch clamp; cytochalasin D; phalloidin; colchicine; taxol


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