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This Article Full Text Full Text (PDF) All Versions of this Article: 293/1/H574    most recent 00205.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Wagenseil, J. E. Articles by Mecham, R. P. Search for Related Content PubMed PubMed Citation Articles by Wagenseil, J. E. Articles by Mecham, R. P.

Elastin-insufficient mice show normal cardiovascular remodeling in 2K1C hypertension despite higher baseline pressure and unique cardiovascular architecture

¹Department of Cell Biology and Physiology, Washington University School of Medicine, Saint Louis, Missouri; and ²Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah

Submitted 15 February 2007 ; accepted in final form 29 March 2007

Mice heterozygous for the elastin gene (ELN^+/–) show unique cardiovascular properties, including increased blood pressure and smaller, thinner arteries with an increased number of lamellar units. Some of these properties are also observed in humans with supravalvular aortic stenosis, a disease caused by functional heterozygosity of the elastin gene. The arterial geometry in ELN^+/– mice is contrary to the increased thickness that would be expected in an animal demonstrating hypertensive remodeling. To determine whether this is due to a decreased capability for cardiovascular remodeling or to a novel adaptation of the ELN^+/– cardiovascular system, we increased blood pressure in adult ELN^+/+ and ELN^+/– mice using the two-kidney, one-clip Goldblatt model of hypertension. Successfully clipped mice have a systolic pressure increase of at least 15 mmHg over sham-operated animals. ELN^+/+ and ELN^+/–-clipped mice show significant increases over sham-operated mice in cardiac weight, arterial thickness, and arterial cross-sectional area with no changes in lamellar number. There are no significant differences in most mechanical properties with clipping in either genotype. These results indicate that ELN^+/+ and ELN^+/– hearts and arteries remodel similarly in response to adult induced hypertension. Therefore, the cardiovascular properties of ELN^+/– mice are likely due to developmental remodeling in response to altered hemodynamics and reduced elastin levels.

arterial mechanics; extracellular matrix; high blood pressure; cardiac hypertrophy; two-kidney, one-clip hypertension