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Articles in PresS, published online ahead of print September 12, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00295.2002
Submitted on May 24, 2002
Accepted on September 4, 2002
1 Department of Internal Medicine, University of California, School of Medicine, Davis, CA, USA
2 Department of Pharmacology, Berlex Biosciences, Richmond, CA, USA
3 Department of Pathology, Microbiology and Immunology, University of California, School of Veterinary Medicine, Davis, CA, USA
* To whom correspondence should be addressed. E-mail: dmtham{at}ucdavis.edu.
Cardiovascular diseases, such as atherosclerosis and hypertension, are associated with arterial stiffening. Previous studies have shown that angiotensin II (Ang II) exacerbated atherosclerosis and induced hypertension and aneurysm formation in apolipoprotein E-deficient (apoE-KO)mice. The aim of the present study was to examine the effects of chronic treatment of Ang II on the arterial elastic properties in apoE-KO mice. We hypothesized that Ang II will injure the arterial wall resulting in increased arterial stiffening. Male apoE-KO mice were infused with either Ang II (1.44 mg/kg/day) or vehicle (phosphate-buffered saline) for 30 days. Ang II treatment accelerated atherosclerosis in the carotid artery by 6-fold (P<0.001) and increased blood pressure by 30% (P<0.05). Additionally, our data demonstrated that Ang II increased arterial stiffening utilizing both in vivo and in vitro methods. Ang II significantly increased pulse wave velocity by 36% (P<0.01) and decreased arterial elasticity as demonstrated by a more than 900% increase in maximal stiffening (high strain Young's modulus) compared to vehicle (P<0.05). These functional changes were correlated with morphological and biochemical changes as demonstrated by an increase in collagen content (60%), a decrease in elastin content (74%), and breaks in the internal elastic lamina in the aortic wall. In addition, endothelium-independent vasorelaxation to sodium nitroprusside was impaired in the aortic rings of Ang II-treated mice compared to vehicle. Thus, the present data indicate that Ang II injures the artery wall in multiple ways and arterial stiffening may be a common outcome of Ang II-induced arterial damage.
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