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Eplerenone with valsartan effectively reduces atherosclerotic lesion by attenuation of oxidative stress and inflammation.
Arterioscler Thromb Vasc Biol. 2006 Apr; 26(4):917-21.AT

Abstract

OBJECTIVE

Angiotensin II contributes to atherogenesis, mainly through oxidative stress and inflammation. Recent data suggest that aldosterone is implicated in some effects of angiotensin II. We hypothesized that aldosterone could directly contribute to oxidative stress and atherosclerotic lesion formation.

METHODS AND RESULTS

Male apolipoprotein E-deficient mice 6 weeks of age were placed on a normal diet or 1.25% high-cholesterol diet. After 6 weeks of the high-cholesterol diet, a marked increase in atherosclerotic lesion formation was observed in the aorta, accompanied by significant elevation of plasma cholesterol level. Production of superoxide anion and expression of NAD(P)H oxidase subunit p47phox, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 in the aorta were increased with the high-cholesterol diet. Eplerenone (1.67 g/kg in high-cholesterol diet) did not affect blood pressure or plasma cholesterol but decreased the atherosclerotic area by nearly 70% (P<0.05), associated with attenuation of oxidative stress and inflammatory response. Valsartan (0.5 mg/kg per day) also decreased the atherosclerotic lesion, whereas coadministration of valsartan and eplerenone further decreased it. Moreover, aldosterone (0.1 micromol/L) enhanced NADPH oxidase activity in cultured vascular smooth muscle cells.

CONCLUSIONS

These results suggest that aldosterone may play a critical role in atherogenesis subsequent to oxidative stress in part independent of angiotensin II-mediated signaling, and that eplerenone could prevent atherosclerosis by attenuating oxidative stress and inflammation.

Authors+Show Affiliations

Division of Medical Biochemistry and Cardiovascular Biology, Department of Molecular and Cellular Biology, Ehime University School of Medicine, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16424347

Citation

Suzuki, Jun, et al. "Eplerenone With Valsartan Effectively Reduces Atherosclerotic Lesion By Attenuation of Oxidative Stress and Inflammation." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 26, no. 4, 2006, pp. 917-21.
Suzuki J, Iwai M, Mogi M, et al. Eplerenone with valsartan effectively reduces atherosclerotic lesion by attenuation of oxidative stress and inflammation. Arterioscler Thromb Vasc Biol. 2006;26(4):917-21.
Suzuki, J., Iwai, M., Mogi, M., Oshita, A., Yoshii, T., Higaki, J., & Horiuchi, M. (2006). Eplerenone with valsartan effectively reduces atherosclerotic lesion by attenuation of oxidative stress and inflammation. Arteriosclerosis, Thrombosis, and Vascular Biology, 26(4), 917-21.
Suzuki J, et al. Eplerenone With Valsartan Effectively Reduces Atherosclerotic Lesion By Attenuation of Oxidative Stress and Inflammation. Arterioscler Thromb Vasc Biol. 2006;26(4):917-21. PubMed PMID: 16424347.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Eplerenone with valsartan effectively reduces atherosclerotic lesion by attenuation of oxidative stress and inflammation. AU - Suzuki,Jun, AU - Iwai,Masaru, AU - Mogi,Masaki, AU - Oshita,Akira, AU - Yoshii,Toyofumi, AU - Higaki,Jitsuo, AU - Horiuchi,Masatsugu, Y1 - 2006/01/19/ PY - 2006/1/21/pubmed PY - 2006/7/15/medline PY - 2006/1/21/entrez SP - 917 EP - 21 JF - Arteriosclerosis, thrombosis, and vascular biology JO - Arterioscler Thromb Vasc Biol VL - 26 IS - 4 N2 - OBJECTIVE: Angiotensin II contributes to atherogenesis, mainly through oxidative stress and inflammation. Recent data suggest that aldosterone is implicated in some effects of angiotensin II. We hypothesized that aldosterone could directly contribute to oxidative stress and atherosclerotic lesion formation. METHODS AND RESULTS: Male apolipoprotein E-deficient mice 6 weeks of age were placed on a normal diet or 1.25% high-cholesterol diet. After 6 weeks of the high-cholesterol diet, a marked increase in atherosclerotic lesion formation was observed in the aorta, accompanied by significant elevation of plasma cholesterol level. Production of superoxide anion and expression of NAD(P)H oxidase subunit p47phox, tumor necrosis factor-alpha, and monocyte chemoattractant protein-1 in the aorta were increased with the high-cholesterol diet. Eplerenone (1.67 g/kg in high-cholesterol diet) did not affect blood pressure or plasma cholesterol but decreased the atherosclerotic area by nearly 70% (P<0.05), associated with attenuation of oxidative stress and inflammatory response. Valsartan (0.5 mg/kg per day) also decreased the atherosclerotic lesion, whereas coadministration of valsartan and eplerenone further decreased it. Moreover, aldosterone (0.1 micromol/L) enhanced NADPH oxidase activity in cultured vascular smooth muscle cells. CONCLUSIONS: These results suggest that aldosterone may play a critical role in atherogenesis subsequent to oxidative stress in part independent of angiotensin II-mediated signaling, and that eplerenone could prevent atherosclerosis by attenuating oxidative stress and inflammation. SN - 1524-4636 UR - https://www.unboundmedicine.com/medline/citation/16424347/Eplerenone_with_valsartan_effectively_reduces_atherosclerotic_lesion_by_attenuation_of_oxidative_stress_and_inflammation_ L2 - https://www.ahajournals.org/doi/10.1161/01.ATV.0000204635.75748.0f?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -