Effect of Peroxisome Proliferator–Activated Receptor-α and -γ Activators on Vascular Remodeling in Endothelin-Dependent Hypertension
Autor: | Marc Iglarz, Rhian M. Touyz, Marie-France Lavoie, Ernesto L. Schiffrin, Quy N. Diep, Farhad Amiri |
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Rok vydání: | 2003 |
Předmět: |
Male
medicine.medical_specialty Vasodilator Agents Receptors Cytoplasmic and Nuclear Peroxisome proliferator-activated receptor Blood Pressure In Vitro Techniques Biology Rats Sprague-Dawley Rosiglitazone Fenofibrate In vivo Internal medicine medicine Animals RNA Messenger Protein Precursors Receptor chemistry.chemical_classification Rats Inbred Dahl Endothelin-1 Activator (genetics) Endothelins Body Weight Endothelin 1 Extracellular Matrix Mesenteric Arteries Rats Oxygen Thiazoles Endocrinology chemistry Hypertension Thiazolidinediones Vascular Resistance Tunica Media Cardiology and Cardiovascular Medicine Endothelin receptor Transcription Factors medicine.drug |
Zdroj: | Arteriosclerosis, Thrombosis, and Vascular Biology. 23:45-51 |
ISSN: | 1524-4636 1079-5642 |
Popis: | 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-γ activator (rosiglitazone, 5 mg · kg −1 · d −1 ), or DOCA-salt+PPAR-α 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 P P Conclusions— PPAR-α and -γ activators were able to modulate endogenous production of ET-1 and had beneficial vascular effects in endothelin-dependent hypertension. |
Databáze: | OpenAIRE |
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