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Articles in PresS, published online ahead of print March 22, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00469.2001
Submitted on December 11, 2001
Accepted on March 18, 2002
1 Medicine, Johns Hopkins University, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: shimodal{at}welch.jhu.edu.
Endothelial barrier dysfunction is typically triggered by increased intracellular Ca2+ concentration. Membrane permeable analogues of cGMP prevent disruption of endothelial cell integrity. Since membrane potential (Em), which influences the electrochemical gradient for Ca2+ influx, is regulated by K+ channels we investigated the effect of 8-bromo-cGMP on Em and inwardly rectifying K+ (KIR) currents in bovine pulmonary artery and microvascular endothelial cells (BPAEC and BMVEC) using whole-cell patch-clamp techniques. Both cell types exhibited inward currents at potentials negative to -50 mV that were abolished by application of 10 µM Ba2+, consistent with KIR current. Ba2+ also depolarized both cell types. 8-bromo-cGMP (10-3 M) depolarized BPAEC and BMVEC, and inhibited KIR current. Pretreatment with RP-8-cPCT-cGMPS or KT 5823, protein kinase G (PKG) antagonists, did not prevent current inhibition by 8-bromo-cGMP. These data suggest that 8-bromo-cGMP induces depolarization in BPAEC and BMVEC due, in part, to PKG-independent inhibition of KIR current. The depolarization could be a protective mechanism that prevents endothelial cell barrier dysfunction by reducing the driving force for Ca2+ entry.
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