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1 Department of Physiology and Biophysics, College of Medicine, Inje University, Busan 614-735; 2 Department of Molecular Science and Technology/Life Science, Ajou University, Suwon 442-749; and 3 National Research Laboratory for Cellular Signaling and Department of Physiology, College of Medicine, Seoul National University, Seoul 110-799, Korea
The present
investigation tested the hypothesis that nitric oxide (NO) potentiates
ATP-sensitive K+ (KATP) channels by protein
kinase G (PKG)-dependent phosphorylation in rabbit ventricular myocytes
with the use of patch-clamp techniques. Sodium nitroprusside (SNP; 1 mM) potentiated KATP channel activity in cell-attached
patches but failed to enhance the channel activity in either inside-out
or outside-out patches. The 8-(4-chlorophenylthio)-cGMP Rp isomer
(Rp-CPT-cGMP, 100 µM) suppressed the potentiating effect of SNP.
8-(4-Chlorophenylthio)-cGMP (8-pCPT-cGMP, 100 µM) increased KATP channel activity in cell-attached patches. PKG (5 U/µl) added together with ATP and cGMP (100 µM each) directly to
the intracellular surface increased the channel activity. Activation of
KATP channels was abolished by the replacement of ATP with
ATP
S. Rp-pCPT-cGMP (100 µM) inhibited the effect of PKG. The
heat-inactivated PKG had little effect on the KATP
channels. Protein phosphatase 2A (PP2A, 1 U/ml) reversed the
PKG-mediated KATP channel activation. With the use of 5 nM
okadaic acid (a PP2A inhibitor), PP2A had no effect on the channel
activity. These results suggest that the NO-cGMP-PKG pathway
contributes to phosphorylation of KATP channels in rabbit
ventricular myocytes.
phosphorylation
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