ArticlePflugers Archiv : European journal of physiology2003
Inhibition of fast sodium current in rabbit ventricular myocytes by protein tyrosine kinase inhibitors.
Article in Pflugers Archiv : European journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 26 citations in OpenAlex.
- Changes in ion channel expression and function associated with cardiac arrhythmogenic remodeling by Sorbs2.Biochimica et biophysica acta. Molecular basis of disease · 2021Article
- Functional cross-talk between phosphorylation and disease-causing mutations in the cardiac sodium channel NaProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Deciphering the Electrophysiological Mechanisms for Ibrutinib-Induced Ventricular Arrhythmias.JACC. CardioOncology · 2020Article
- Genistein Inhibits AβCellular and molecular neurobiology · 2019Article
- Phosphorylation of cardiac voltage-gated sodium channel: Potential players with multiple dimensions.Acta physiologica (Oxford, England) · 2019Review
- SRC tyrosine kinases regulate neuronal differentiation of mouse embryonic stem cells via modulation of voltage-gated sodium channel activity.Neurochemical research · 2015Article
- Genistein inhibits voltage-gated sodium currents in SCG neurons through protein tyrosine kinase-dependent and kinase-independent mechanisms.Pflugers Archiv : European journal of physiology · 2008Article
- Lipid bilayer-mediated regulation of ion channel function by amphiphilic drugs.The Journal of general physiology · 2008Article
- Directed molecular screening for RecA ATPase inhibitors.Bioorganic & medicinal chemistry letters · 2007Article
- Insensitivity of cardiac delayed-rectifier I(Kr) to tyrosine phosphorylation inhibitors and stimulators.British journal of pharmacology · 2006Article
- Ultraviolet photoalteration of late Na+ current in guinea-pig ventricular myocytes.The Journal of membrane biology · 2006Article
- Early painful diabetic neuropathy is associated with differential changes in tetrodotoxin-sensitive and -resistant sodium channels in dorsal root ganglion neurons in the rat.The Journal of biological chemistry · 2004Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The present study investigated the effects of protein tyrosine kinase inhibitors on the fast sodium current ( I(Na)) in rabbit ventricular myocytes. Single rabbit ventricular myocytes were isolated enzymatically using Langendorff perfusion. I(Na) was recorded using the whole-cell patch-clamp technique at room temperature. The protein tyrosine kinase inhibitors genistein, AG957, ST638, and PP2 reversibly inhibited I(Na) in a concentration-dependent manner. At a test pulse potential of -30 mV, genistein (n=7) inhibited I(Na) by 37.7+/-3.2%, 53.4+/-2.5%, and 71.8+/-2.7% at concentrations of 15, 50, and 100 microM, respectively, without changing the voltage dependence of activation, while 100 microM AG957, 100 microM ST638, and 30 microM PP2 inhibited I(Na) by 38.7+/-2.4, 35.8+/-3.4, and 21.1+/-3.9%, respectively. Genistein (100 microM) and AG957 (100 microM) shifted the voltage for half-maximal inactivation of I(Na) from -76.7+/-2.0 mV (n=10) in control to -88.37+/-2.6 mV (n=6, P<0.05), and -82.9+/-1.7 (n=4, P<0.05), respectively, without changing the slope factor. Genistein and AG957 also significantly prolonged the time course of I(Na) recovery from inactivation. Daidzein and PP3, inactive analogs of genistein and PP2, respectively, did not inhibit I(Na) significantly. We conclude that protein tyrosine kinase signaling pathways may play an important role in regulation of I(Na) in cardiac myocytes.
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