Donate Help Contact The AHA Sign In Home
American Heart Association
Arteriosclerosis, Thrombosis, and Vascular Biology
Search: search_blue_button Advanced Search
Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:42-48
doi: 10.1161/hq0102.101098
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ryan, M. J.
Right arrow Articles by Sigmund, C. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ryan, M. J.
Right arrow Articles by Sigmund, C. D.
Related Collections
Right arrow Health policy and outcome research
Right arrow Acute coronary syndromes
Right arrow CV surgery: aortic and vascular disease
Right arrow CV surgery: transplantation, ventricular assistance, cardiomyopathy
Right arrow Genetics of Stroke
(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:42.)
© 2002 American Heart Association, Inc.


Vascular Biology

Endothelial Dysfunction and Blood Pressure Variability in Selected Inbred Mouse Strains

Michael J. Ryan; Sean P. Didion; Deborah R. Davis; Frank M. Faraci; Curt D. Sigmund

From the Department of Internal Medicine (M.J.R., S.P.D., D.R.D., F.M.F., C.D.S.), Department of Pharmacology (F.M.F.), and Department of Physiology and Biophysics (C.D.S.), Cardiovascular Center, University of Iowa, Iowa City.

Correspondence to Curt D. Sigmund, PhD, Professor of Internal Medicine, 2191 Medical Laboratories, University of Iowa, Department of Internal Medicine, Iowa City, IA 52242. E-mail Curt-Sigmund{at}uiowa.edu

The genetic regulation of blood pressure (BP) and endothelial function is likely to be polygenic. Because there is considerable variability in basal BP among inbred mouse strains, the purpose of this study was to determine whether a similar variability in vascular function exists among 7 "normotensive" strains. We tested the hypothesis that compared with mice with higher BPs, mice with lower BPs would have greater aortic endothelial responses to acetylcholine (ACh). Mean BP ranged from 117 to 145 mm Hg among the 7 strains. The responses of aortic rings to ACh, sodium nitroprusside, and papaverine were assessed after submaximal precontraction with prostaglandin F2{alpha}. The aortas from all strains relaxed in a concentration-dependent manner to sodium nitroprusside and papaverine, but responses to ACh were markedly impaired in the aortas, but not carotid arteries, from 129P3/J and 129X1/SvJ mice. Aortas from the other strains relaxed normally to ACh. Furthermore, the endothelium-dependent dilators ADP and A23187 caused similar relaxation in 129P3/J, 129X1/SvJ, and C57BL/6J mice. Although the data do not support the initial hypothesis, the impaired aortic response to ACh in the 129 strains is a novel finding and illustrates the potential impact that genetic background can have on vascular responsiveness.


Key Words: aorta • blood pressure • endothelium • inbred mice