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 DDAuthor
David Gutterman MD Emeritus Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAorta, Abdominal
Arteriosclerosis
Endothelium, Vascular
Hypercholesterolemia
Lipoproteins, LDL
Potassium Channels
Rabbits
Vasodilation
