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Am J Physiol Heart Circ Physiol (July 26, 2002). doi:10.1152/ajpheart.00326.2002
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Articles in PresS, published online ahead of print July 26, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00326.2002
Submitted on April 10, 2002
Accepted on July 24, 2002

G Protein Modulates Thyroid Hormone Induced Sodium Channel Activation in Ventricular Myocytes

Luyi Sen1*, Yoshihide Sakaguchi1, and Guanggen Cui1

1 Medicine/Cardiology, UCLA Medical Center/UCLA School of Medicine, Los Angeles, CA, USA

* To whom correspondence should be addressed. E-mail: lsen{at}mednet.ucla.edu.

T3 (1nM) acutely increased whole-cell INa and shifted the steady-state inactivation curve in a dose-dependent manner. This effect was reproduced by TAA and blocked by rT3. When the pipette solution contained 100 µM GTP or GTP{gamma}S, T3 effects on the whole-cell INa current were increased 2-3 fold. This effect was almost completely abolished by pertusis toxin pre-incubation. In cell-attached patch, T3 increased the open probability of single INa channel by reducing the null probability without changing the mean open time and the number of available channels. In inside-out patch configuration, the effect of T3 while GTP{gamma}S was present was 10 times faster than that in whole cell and cell-attached patches, and could be completely washed out. Without GTP{gamma}S, 10 nM T3 only slightly increased the channel open probability by increasing rate constant kCO, and reducing the null probability. GTP{gamma}S exposure only increased the number of functional channels. T3 (10 nM) and GTP{gamma}S (10µM) synergistically enhanced the channel open probability 5.8±0.5 fold by increasing kCO, decreasing kOI and greatly reducing PN.




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