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Cardiovascular Research Advance Access [Accepted Manuscript] published online on October 30, 2007
Cardiovascular Research, doi:10.1093/cvr/cvm055
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Alteration in flow (shear stress)-induced remodeling in rat resistance arteries with aging: improvement by a treatment with hydralazine

Odile Dumont*, Frederic Pinaud*,#, Anne-Laure Guihot*, Christophe Baufreton#, Laurent Loufrani* and Daniel Henrion*,

* CNRS UMR 6214, INSERM U771, University of Angers, Angers, France
# UPRES-EA 3860, CHU d'Angers, University of Angers, Angers, France

Address for Correspondence: Dr. Daniel Henrion, Pharm.D., Ph.D. UMR CNRS6214-INSERM771, Faculté de Médecine, 49045 Angers, FRANCE tel: 332 41 73 58 45 fax: 332 41 73 58 95 E-mail: daniel.henrion{at}univ-angers.f

Aim: The link between aging and vascular diseases remains unclear, especially in resistance arteries. As a decreased vasodilator capacity of the endothelium is usually described in aging, we hypothesized that arteriolar remodeling in response to a chronic increase in blood flow might be altered. In addition, we tested the capacity of a vasodilator treatment with hydralazine to restore remodeling, as we have previously shown that hydralazine has a potent effect on the process.

Methods: Mesenteric resistance arteries (350 µm diameter) from 3-month- and 24-month-old rats were exposed to high (HF) and normal blood flow (NF), for 2 weeks by sequentially ligating second-order arteries in vivo.

Results: In HF arteries, diameter increased by 21% when intraluminal pressure was 100 mmHg, in association with a rise in superoxide production in young rats. On the other hand, both diameter and superoxide levels failed to increase in old rats. Hydralazine restored HF-induced remodeling in old rats in association with an increased superoxide production and a decreased superoxide dismutase (SOD) expression. The SOD mimetic TEMPOL prevented the effect of hydralazine on the arterial diameter. In old rats hydralazine increased arterial diameter in HF arteries without increasing eNOS expression. Furthermore, hydralazine also restored HF remodeling in eNOS knockout mice.

Conclusion: Thus, flow remodeling in resistance arteries failed to occur in aging but it could be restored by hydralazine via a reactive oxygen species (ROS)-dependent mechanism. These findings may have serious pathophysiological consequences in situations requiring flow-dependent remodeling such as ischemic and metabolic diseases, more frequent in the elderly.

KEYWORDS Microcirculation; remodeling; blood flow; aging; nitric oxide; reactive oxygen species

Time for primary review: 23


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