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Am J Physiol Heart Circ Physiol (October 10, 2008). doi:10.1152/ajpheart.00155.2008
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Submitted on February 13, 2008
Revised on September 21, 2008
Accepted on October 6, 2008

Heightened Aberrant Deposition of Hard-Wearing Elastin in Conduit Arteries of Pre-hypertensive SHR is Associated with Increased Stiffness and Inward Remodeling

Silvia M Arribas1*, Ana Maria Briones1, Catherine Bellingham2, M. Carmen Gonzalez1, Mercedes Salaices3, Kela Liu4, Yanting Wang4, and Aleksander Hinek4

1 Universidad Autonoma de Madrid
2 Hospital for Sick Children, University of Toronto
3 Universidad Autnoma de Madrid
4 The Hospital for Sick Children. University of Toronto

* To whom correspondence should be addressed. E-mail: silvia.arribas{at}uam.es.

Elastin is a major component of conduit arteries and a key determinant of vascular visco-elastic properties. Aberrant organization of elastic lamellae has been reported in resistance vessels from spontaneously hypertensive rats (SHR) prior to the development of hypertension. Hence, we have characterized the content and organization of elastic lamellae in conduit vessels of neonatal SHR in detail, comparing the carotid arteries from one week-old SHR with those from Wistar Kyoto (WKY) and Sprague Dawley (SD) rats. The general structure and mechanics were studied by pressure myography, and the internal elastic lamina organization was determined by confocal microscopy. Cyanide bromide-insoluble elastin scaffolds were also prepared from one month-old SHR and WKY aortas to assess their weight, amino-acid composition, three-dimensional lamellar organization and mechanical characteristics. Carotid arteries from 1 week-old SHR exhibited narrower lumen and greater intrinsic stiffness than those from their WKY and SD counterparts. These aberrations were associated with heightened elastin content and with a striking reduction in the size of the fenestrae present in the elastic lamellae. The elastin scaffolds isolated from SHR aortas also exhibited increased relative weight and stiffness, as well as the presence of peculiar trabeculae inside the fenestra that reduced their size. We suggest that the excessive and aberrant elastin deposited in SHR vessels during perinatal development alters their mechanical properties. Such abnormalities are likely to compromise vessel expansion during a critical period of growth and, at later stages, they could compromise hemodynamic function and participate in the development of systemic hypertension.




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Am. J. Physiol. Heart Circ. Physiol.Home page
G. Weissen-Plenz and J. R. Sindermann
Letter to the editor: "Looking for molecular mechanisms underlying aberrant elastin deposition in hypertension"
Am J Physiol Heart Circ Physiol, March 1, 2009; 296(3): H900 - H900.
[Full Text] [PDF]


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Am. J. Physiol. Heart Circ. Physiol.Home page
A. Hinek
Reply to "Letter to the editor: 'Looking for molecular mechanisms underlying aberrant elastin deposition in hypertension'"
Am J Physiol Heart Circ Physiol, March 1, 2009; 296(3): H901 - H901.
[Full Text] [PDF]




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