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Vol. 61, Issue 2, 285-293, February 2002
Department of Physiology and Cell Biology, University of Nevada
School of Medicine, Reno, Nevada
The regulation of cardiac delayed rectifier potassium (Kv) currents by
cAMP-dependent protein kinase (PKA) contributes to the control of blood
pressure and heart rate. We investigated the modulation by PKA and
protein phosphatases of cloned Kv1.5 channels expressed in
Xenopus laevis oocytes. Exposure of oocytes to
activators of PKA (100 nM forskolin, 1 mM 8-bromo-cAMP, or 1 mM
3-isobutyl-1-methylxanthine) had no effect on the amplitude of Kv1.5
currents. Inhibition of PKA by injection of protein kinase A inhibitor
peptide or exposure to myristoylated protein kinase A inhibitor peptide
(M-PKI; 100 nM) reduced currents mediated by Kv1.5. M-PKI also reduced
the amplitude of currents mediated by mutated Kv1.5 channels in which
the COOH terminal PKA phosphorylation sites and PSD-95, Disc-large, and
ZO-1-binding domain were removed. The reduction of Kv1.5 currents by
M-PKI was attenuated by inhibition of actin polymerization by 1 µM
cytochalasins B and D, but was not affected by 10 µM phalloidin
(stabilizes actin filaments) or 50 µM colchicine (disrupts
microtubules). Treatment of oocytes with antisense oligonucleotides
against 
-actinin-2 abolished the reduction in Kv1.5 current by
M-PKI. These observations suggest that Kv1.5 currents are activated by
endogenous PKA in "resting" oocytes and that inhibition of PKA
activity reveals the action of endogenous phosphatases. Indeed,
injection of alkaline phosphatase reduced currents mediated by Kv1.5.
Further preincubation of oocytes with 1 mM sodium orthovanadate (a
protein tyrosine phosphatase inhibitor) abolished the reduction in
Kv1.5 currents by M-PKI. We conclude that currents encoded by Kv1.5 are
regulated by PKA and protein tyrosine phosphatase and that this
regulation requires an intact actin cytoskeleton and -actinin-2.
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