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Endothelium-derived hyperpolarizing factor mediated relaxations in pig coronary arteries do not involve Gi/o proteins.

Abstract：

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 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). 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 alpha2-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.

journal_name

Acta Pharmacol Sin

journal_title

Acta pharmacologica Sinica

authors

Ng KF,Leung SW,Man RY,Vanhoutte PM

doi

10.1111/j.1745-7254.2008.00905.x

subject

Has Abstract

pub_date

2008-12-01 00:00:00

pages

1419-24

issue

12

eissn

1671-4083

issn

1745-7254

journal_volume

29

pub_type

杂志文章

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