Open AccessEndothelium‐derived hyperpolarizing factor mediated relaxations in pig coronary arteries do not involve Gi/o proteins 1,2
Author(s) -
NG Kwok Fu Jacobus,
LEUNG Susan Wai Sum,
MAN Ricky Ying Keung,
VANHOUTTE Paul M
Publication year - 2008
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2008.00905.x
Subject(s) - pertussis toxin , apamin , endothelium derived hyperpolarizing factor , bradykinin , charybdotoxin , chemistry , g protein , nitric oxide , medicine , agonist , endocrinology , pharmacology , receptor , biochemistry , calcium
Aim: 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). Methods: Pig coronary arterial rings with endothelia were suspended in organ chambers filled with Krebs‐Ringer bicarbonate solution maintained at 37 °C and continuously aerated with 95%O 2 and 5% CO 2 . Isometric tension was measured during contractions to prostaglandin F 2α in the presence of indomethacin and N ω ‐nitro‐ L ‐arginine methyl ester ( L ‐NAME). Results: 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 α2‐adrenergic agonist UK14304 and those to serotonin were abolished in the presence of indomethacin and L ‐NAME. Conclusion: 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.