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Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:45-51
Published online before print November 14, 2002, doi: 10.1161/01.ATV.0000047447.67827.CD
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:45.)
© 2003 American Heart Association, Inc.

Vascular Biology

Effect of Peroxisome Proliferator–Activated Receptor-{alpha} and -{gamma} Activators on Vascular Remodeling in Endothelin-Dependent Hypertension

Marc Iglarz; Rhian M. Touyz; Farhad Amiri; Marie-France Lavoie; Quy N. Diep; Ernesto L. Schiffrin

From the CIHR Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, University of Montreal, Montreal, Quebec, Canada.

Correspondence to Ernesto L. Schiffrin, MD, PhD, FRCPC, Clinical Research Institute of Montreal, 110 Pine Ave W, Montreal, Quebec, Canada H2W 1R7. E-mail schiffe{at}ircm.qc.ca

Objective— Peroxisome proliferator–activated receptors (PPARs) may modulate in vitro the vascular production of vasoactive peptides such as endothelin-1 (ET-1). Thus, we investigated in vivo the interaction between PPARs and ET-1 in deoxycorticosterone acetate (DOCA)–salt rats that overexpress vascular ET-1.

Methods and Results— Unilaterally nephrectomized 16-week-old Sprague-Dawley rats (Uni-Nx) were divided into 4 groups (n=6 each): control group, DOCA-salt group, DOCA-salt+PPAR-{gamma} activator (rosiglitazone, 5 mg · kg-1 · d-1), or DOCA-salt+PPAR-{alpha} activator (fenofibrate, 100 mg · kg-1 · d-1). Systolic blood pressure was significantly increased in the DOCA-salt group (240±11 vs 121±2 mm Hg in Uni-Nx, P<0.01). Progression of hypertension was partially prevented by coadministration of rosiglitazone (172±3 mm Hg vs DOCA-salt, P<0.05) but not by fenofibrate. Both PPAR activators abrogated the increase in prepro-ET-1 mRNA content in the mesenteric vasculature of DOCA-salt rats. The media-to-lumen ratio was increased in DOCA-salt rats (10.3±0.9% vs 4.9±0.5% in Uni-Nx rats, P<0.01). Rosiglitazone and fenofibrate prevented the hypertrophic remodeling observed in DOCA-salt rats without affecting vascular stiffness. Rosiglitazone but not fenofibrate prevented endothelial dysfunction in pressurized mesenteric arteries. Finally, both rosiglitazone and fenofibrate prevented the vascular increase in superoxide anion production induced in DOCA-salt animals.

Conclusions— PPAR-{alpha} and -{gamma} activators were able to modulate endogenous production of ET-1 and had beneficial vascular effects in endothelin-dependent hypertension.


Key Words: PPAR activators • rosiglitazone • fenofibrate • resistance arteries • DOCA-salt




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