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Alterations in structure and mechanics of resistance arteries from ouabain-induced hypertensive rats.

Briones AM, Xavier FE, Arribas SM, González MC, Rossoni LV, Alonso MJ, Salaices M

Departamento de Farmacología y Terapéutica, Facultad de Medicina, Universidad Autónoma de Madrid, C/Arzobispo Morcillo, E-28029 Madrid, Spain.

We have previously described that chronic administration of ouabain induces hypertension and functional alterations in mesenteric resistance arteries. The aim of this study was to analyze whether ouabain treatment also alters the structural and mechanical properties of mesenteric resistance arteries. Wistar rats were treated for 5 wk with ouabain (8.0 microg/day sc). The vascular structure and mechanics of the third-order branches of the mesenteric artery were assessed with pressure myography and confocal microscopy. Total collagen content was determined by picrosirius red staining, collagen I/III was analyzed by Western blot, and elastin was studied by confocal microscopy. Vascular reactivity was analyzed by wire myography. Internal and external diameters and cross-sectional area were diminished, whereas the wall-to-lumen ratio was increased in arteries from ouabain-treated rats compared with controls. In addition, arteries from ouabain-treated rats were stiffer. Ouabain treatment decreased smooth muscle cell number and increased total and I/III collagens in the vascular wall. However, this treatment did not modify adventitia and media thickness, nuclei morphology, elastin structure, and vascular reactivity to norepinephrine and acetylcholine. The present work shows hypotrophic inward remodeling of mesenteric resistance arteries from ouabain-treated rats that seems to be the consequence of a combination of decreased cell number and impaired distension of the artery, possibly due to a higher stiffness associated with collagen deposition. The narrowing of resistance arteries could play a role in the pathogenesis of hypertension in this model.

Published 14 June 2006 in Am J Physiol Heart Circ Physiol, 291(1): H193-201.
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