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Updated: Apr 6, 2026
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Sex Difference in Coronary Endothelial Dysfunction in Apolipoprotein E Knockout Mouse: Role of NO and A2A Adenosine
Xueping Zhou1,2, Bunyen Teng1,2, S J Mustafa1,2
1Department of Physiology and Pharmacology, West Virginia University, Morgantown, West Virginia, USA.
Objective:
Sex plays an important role in the pathophysiology of cardiovascular diseases. This study aims to investigate how sex impacts on the coronary flow regulation during atherosclerosis.
Methods:
ApoE KO mouse fed with western diet were used for atherosclerosis model. Coronary RH and flow response were measured using Langendorff-perfused isolated hearts.
Results:
Coronary RH and A23187-induced NO-dependent flow increases were significantly reduced in female (by ~28% and 48%, respectively), but not in male atherosclerotic mice. However, SNP-induced coronary vasodilation remains intact in both sexes of ApoE KO mice. L-NAME (NOS inhibitor) reduced baseline flow and RH to a lesser extent in ApoE KO (by ~19% and 31%) vs. WT (~30% and 59%, respectively), and abolished the sex difference in RH. In contrast, SCH58261 (a selective A2A AR antagonist) reduced the baseline flow and RH to a greater extent in atherosclerotic mice, but did not affect the sex difference. Immunofluorescent staining of coronary arteries showed a similar A2A AR upregulation in both sexes of ApoE KO mice.
Conclusions:
Our results suggest that during atherosclerosis, female mice are more susceptible to NO-dependent endothelial dysfunction and the upregulation of A2A AR may serve as a compensatory mechanism to counteract the compromised endothelial function.
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