Effect of ouabain on endothelium-dependent relaxation of human resistance arteries.
Inhibition of active sodium transport by ouabain was found to cause concentration- and time-dependent impairment of acetylcholine-induced relaxation in human resistance arteries with a significant effect at 100 pM. The reduced acetylcholine response was attributable to inhibition of the NG-monomethyl L-arginine-sensitive but not the indomethacin-sensitive component of relaxation. Relaxation by sodium nitroprusside was not affected by ouabain, suggesting that inhibition of sodium transport, directly or indirectly, must affect synthesis or release of endothelium-derived relaxing factor rather than its effector pathway. These results do not support the existence of an additional endothelium-derived relaxing factor other than endothelium-derived relaxing factor, which is dependent on sodium pump activity. The finding that inhibition of sodium transport has a profound effect on vascular relaxation may have implications in the pathogenesis of certain forms of hypertension.
Woolfson
R G
RG
Department of Physiology, St Thomas' Hospital, London, England.
Poston
L
L
D000109:Acetylcholine / Q000494:pharmacology; D001120:Arginine / Q000031:analogs & derivatives / Q000494:pharmacology; D001158:Arteries / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000502:physiology*; D005260:Female; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D009599:Nitroprusside / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology*; D014655:Vascular Resistance; D014664:Vasodilation / Q000187:drug effects*; D019323:omega-N-Methylarginine
D009599:Nitroprusside; D019323:omega-N-Methylarginine; D010042:Ouabain; D001120:Arginine; D000109:Acetylcholine; D007213:Indomethacin