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  • Title: Cyclic AMP mediates EDHF-type relaxations of rabbit jugular vein.
    Author: Griffith TM, Taylor HJ.
    Journal: Biochem Biophys Res Commun; 1999 Sep 16; 263(1):52-7. PubMed ID: 10486252.
    Abstract:
    Isolated rings of rabbit jugular vein have been used to test the hypothesis that formation of cAMP within the endothelial cell contributes to relaxations that are attributable to the endothelium-derived hyperpolarizing factor, EDHF. Relaxations induced by acetylcholine under conditions of combined NO synthase and cyclooxygenase blockade were almost abolished by inhibition of adenylate cyclase with the selective P-site agonist 2', 3'-dideoxyadenosine (2',3'-DDA). They were similarly attenuated by the gap junction inhibitors 18alpha-glycyrrhetinic acid (18alpha-GA) and Gap 27 peptide which interrupt direct endothelium-smooth muscle communication without themselves affecting smooth muscle tone. By contrast, stimulation of adenylate cyclase with forskolin promoted gap junction-dependent relaxations, with concentration-relaxation curves to this agent exhibiting an equivalent rightward shift in the presence of 18alpha-GA and following endothelial denudation. The findings suggest that cAMP may cross from the endothelium to smooth muscle via gap junction channels and/or enhance the endothelial hyperpolarization normally associated with agonist stimulation. Both mechanisms may contribute to EDHF/gap junction-dependent relaxations.
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