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Articles in PresS, published online ahead of print May 16, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01052.2001
Submitted on December 3, 2001
Accepted on May 6, 2002
1 Department of Physiology and Biophysics, College of Medicine, Inje University, Busan, Korea, Republic of
2 Department of Molecular Science & Technology/Life Science, Ajou University, Suwon, Korea, Republic of
3 National Research Laboratory for Cellular Signaling and Department of Physiology and Biophysics, College of Medicine, Seoul National University, Seoul, Korea, Republic of
* To whom correspondence should be addressed. E-mail: phyhanj{at}ijnc.inje.ac.kr.
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 using the 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. 8-(4-Chlorophenylthio)-guanosine-3',5'-cyclic monophosphate, Rp-isomer (Rp-CPT-cGMP, 100 µM) suppressed the potentiating effect of SNP. 8-(4-Chlorophenylthio)-guanosine-3',5'-cyclic monophosphate (8-pCPT-cGMP, 100 µM) increased KATP channel activity in cell-attached patches. PKG (5 U/ml) 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 replacing 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, 1U/ml) reversed the PKG-mediated KATP channel activation. In the presence of okadaic acid (OA, 5 nM), a PP2A inhibitor, PP2A had no effect on the channel activity. These results suggest that NO/cGMP/PKG-pathway contributes to phosphorylation of KATP channels in rabbit ventricular myocytes.
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