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- W2077519675 abstract "Endothelium-dependent relaxations to certain neurohumoral substances are mediated by pertussis toxin-sensitive Gi/o protein. Our experiments were designed to determine the role, if any, of pertussis toxin-sensitive G-proteins in relaxations attributed to endothelium-derived hyperpolarizing factor (EDHF).Pig coronary arterial rings with endothelia were suspended in organ chambers filled with Krebs-Ringer bicarbonate solution maintained at 37 degrees and continuously aerated with 95%O2 and 5% CO2. Isometric tension was measured during contractions to prostaglandin F2alpha in the presence of indomethacin and N(omega)- nitro-L-arginine methyl ester (L-NAME).Thrombin, the thrombin receptor- activating peptide SFLLRN, bradykinin, substance P, and calcimycin produced dose-dependent relaxations. These relaxations were not inhibited by prior incubation with pertussis toxin, but were abolished upon the addition of charybdotoxin plus apamin. Relaxations to the alpha2-adrenergic agonist UK14304 and those to serotonin were abolished in the presence of indomethacin and L-NAME.Unlike nitric oxide-mediated relaxations, EDHF-mediated relaxations of pig coronary arteries do not involve pertussis toxin-sensitive pathways and are Gi/o protein independent." @default.
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- W2077519675 date "2008-12-01" @default.
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- W2077519675 title "Endothelium-derived hyperpolarizing factor mediated relaxations in pig coronary arteries do not involve Gi/o proteins" @default.
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- W2077519675 doi "https://doi.org/10.1111/j.1745-7254.2008.00905.x" @default.
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