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. 2017 Jul 12;70(2):401–411. doi: 10.1161/HYPERTENSIONAHA.117.09113

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© 2017 The Authors.

Hypertension is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDerivs License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 5. — Effects of PKA and PKG (protein kinase A and G) inhibitors on cyclic nucleotide–induced gap junction intercellular communication (GJIC). PKA, but not PKG-mediated processes, increased Cx43 (connexin 43) Lucifer yellow dye transfer. Representative fluorescence dye microscopy images: (A) untreated control nonpregnant and pregnant uterine artery endothelial cells (NP-UAECs and P-UAECs), (B) P-UAECs pretreated with 10 μmol/L of either PKA inhibitor (PKI; 1 hour) or PKG inhibitor (Rp-8-Br [8-Bromo]-PET-cGMPs; 1 hour) then 1 mmol/L 8-Br-cAMP for 30 minutes, and (C) P-UAECs pretreated with 10 μmol/L of either PKA inhibitor (PKI; 1 hour) or PKG inhibitor (Rp-8-Br-PET-cGMPs; 1 hour) then 1 mmol/L of 8-Br-cGMP for 30 minutes. Left, Illustrates tetramethylrhodamine (TMR) dextran staining at the cell membrane. TMR dextran is too large to pass through gap junctions (GJs) and, thus, serves as a measure of cell damage at the wounding site and a marker for Lucifer yellow entry. Middle, Illustrates Lucifer yellow dye passing through GJs into adjacent cells. Right, An overlapping merged photo of the TMR dextran and Lucifer yellow dye images. Dotted lines (—) denote the wound site, whereas the extended arrows (|←) denote the distance Lucifer Yellow dye traveled from the wound site.