Tyrphostins increase membrane conductance in ventricular myocytes through a tyrosine kinase-independent mechanism, likely by stimulating Na+-Ca2+ exchange.
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Alerts to off-target tyrphostin effects on myocyte conductance; leaves open their specificity as tyrosine kinase tools in cardiac research.
ABSTRACT-The effects of the tyrosine kinase (TK) inhibitor tyrphostin A23 and its inactive analog tyrphostin Al on background membrane conductance were investigated in guinea pig ventricular myocytes. TK-inhibiting A23 reversibly increased membrane conductance under conditions designed to minimize Na+, Ca2+, K+, and Na+-K+ pump currents. Similar stimulatory action was obtained with TK-inactive Al. The tyrphostin-induced current was inhibited by omitting external Na+ or Ca+, suppressed by chelating internal Ca2+, blocked by external Cd2+ and Ni2+, and insensitive to changes in internal Cl- concentration. We conclude that tyrphostins have a direct, TK-independent action that increases membrane conductance probably by stimulating Na+-Ca2+ exchange.
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Ogura et al. (2001) studied this question.
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