Fibronectin expression and aortic wall elastic modulus in spontaneously hypertensive rats.
Recent studies have shown that large-artery wall remodeling per se does not reduce distensibility in hypertension, indicating qualitative or quantitative changes in arterial components. The aim of the study was to determine in 1-year-old spontaneously hypertensive rats (SHRs) the changes in the elastic properties of large arteries, as assessed by the incremental elastic modulus (E(inc)), and the changes in the extracellular matrix, including fibronectin (FN) and alpha5beta1-integrin. The relationship between E(inc) and circumferential wall stress was calculated from in vivo pulsatile changes in blood pressure and arterial diameter by using a high-resolution echo-tracking system at the site of the abdominal aorta and in vitro medial cross-sectional area. E(inc)-stress curves and FN and integrin alpha5-subunit contents were determined for each animal. Mean stress and E(inc) were higher in SHRs than in Wistar rats. However, in a common range of stress, E(inc)-stress curves for SHRs were superimposable on those for Wistar rats, indicating that wall materials in both strains have equivalent mechanical behavior. Immunohistochemistry indicated that total FN, EIIIA FN isoform, and alpha5-integrin increased in the SHRs aortas without changes in elastin and collagen densities. Total FN was also increased in SHRs as determined by Western blot analysis. No differences in FN and alpha5-subunit mRNAs were detected between SHRs and Wistar rats. These results indicate that the aortic wall material of SHRs and Wistar rats have equivalent mechanical properties, although in SHRs it is subjected to a higher level of stress. By increasing cell-matrix attachment sites, FN may participate in the mechanical adaptation of both cellular and matrix components in SHRs.
Bézie
Y
Y
Institut National de la Santé et de la Recherche Médicale, U337, Paris, France.
Lamazière
J M
JM
Laurent
S
S
Challande
P
P
Cunha
R S
RS
Bonnet
J
J
Lacolley
P
P
D000818:Animals; D015703:Antigens, CD / Q000032:analysis / Q000235:genetics; D001011:Aorta / Q000503:physiopathology*; D015152:Blotting, Northern; D004548:Elasticity; D005109:Extracellular Matrix / Q000502:physiology; D005353:Fibronectins / Q000032:analysis / Q000235:genetics*; D015870:Gene Expression; D006439:Hemodynamics; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology*; D039482:Integrin alpha5; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR; D017208:Rats, Wistar; D013314:Stress, Mechanical
D015703:Antigens, CD; D005353:Fibronectins; D039482:Integrin alpha5