Calcium-activated potassium channels mask vascular dysfunction associated with oxidized LDL exposure in rabbit aorta. Jpn Heart J 2001 May;42(3):317-26
Date
10/19/2001Pubmed ID
11605770DOI
10.1536/jhj.42.317Scopus ID
2-s2.0-0034820290 (requires institutional sign-in at Scopus site) 2 CitationsAbstract
Endothelium-dependent vasodilation is impaired in atherosclerosis. Oxidized low density lipoprotein (ox-LDL) plays an important role, possibly through alterations in G-protein activation. We examined the effect of acute exposure to ox-LDL on the dilator responses of isolated rabbit aorta segments. We sought also to evaluate the specificity of this dysfunction for dilator stimuli that traditionally operate through a Gi-protein mechanism. Aortic segments were prepared for measurement of isometric tension. After contraction with prostaglandin F2alpha, relaxation to thrombin, adenosine diphosphate (ADP), or the endothelium-independent agonists, sodium nitroprusside (SNP) or papaverine was examined. Maximal relaxation to thrombin was impaired in the presence of ox-LDL (17.7+/-3.7% p<0.05) compared to control (no LDL) (52.6+/-4.0%). Ox-LDL did not affect maximal relaxation to ADP or SNP. However, in the presence of charybdotoxin (CHTX: calcium-activated potassium channel inhibitor) ox-LDL impaired relaxation to ADP (17.4+/-3.2%). CHTX did not affect control (no LDL) responses to ADP (69.6+/-5.0%) or relaxation to thrombin or papaverine. In conclusion, ox-LDL impairs relaxation to thrombin, but in the case of ADP, calcium-activated potassium channels compensate to maintain this relaxation.
Author List
Bocker JM, Miller FJ, Oltman CL, Chappell DA, Gutterman DDMESH terms used to index this publication - Major topics in bold
AnimalsAorta, Abdominal
Arteriosclerosis
Endothelium, Vascular
Hypercholesterolemia
Lipoproteins, LDL
Potassium Channels
Rabbits
Vasodilation