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Contribution of different Nox homologues to cardiac remodeling in two-kidney two-clip renovascular hypertensive rats: effect of valsartan.
Pharmacol Res. 2007 May; 55(5):408-17.PR

Abstract

Growing evidences have shown that hypertension, cardiac hypertrophy and fibrosis were associated with an overactivity of NAD(P)H oxidase. It is unknown, however, which isoform of NAD(P)H oxidase yields O(2)*(-) formation in heart and aorta in two-kidney, two-clip (2K2C) hypertensive rats in vivo and thus is responsible for the development of cardiac remodeling. We examined the pathological change of NAD(P)H oxidase homologues and tested the effect of valsartan on the cardiac remodeling in 2K2C renovascular hypertensive rats. Four weeks after male Sprague-Dawley rats accepted 2K2C or sham operation, 2K2C hypertensive (>160 mmHg) rats were divided into vehicle-treated (2K2C) and valsartan (30 mg kg(-1) per day, for 6 weeks)-treated (2K2C+Val) groups, which were compared with sham-operated controls (Sham). At week 10, 2K2C hypertensive rats showed increased serum level of angiotensin II (Ang II), MDA and blood pressure (BP), obvious cardiac hypertrophy and fibrosis, increased O(2)*(-) production and NAD(P)H oxidase activity and expression in aorta and heart. The heart in 2K2C hypertensive rats preferred to use NADH as substrate while the aorta used both NADH and NADPH. Valsartan treatment decreased BP, ameliorated cardiac hypertrophy and fibrosis, decreased O(2)*(-) production and NAD(P)H oxidase activity in aorta and heart. Nox2 and Nox4 protein expression increased in heart, while Nox1 and Nox4 increased in aorta in 2K2C hypertensive rats, which were all normalized after valsartan treatment. In conclusion, these data indicate that different Nox expression might account for substrate preference and the formation of O(2)*(-) by NAD(P)H oxidase resulting from elevated Ang II in the 2K2C model contributes to the development of renovascular hypertension and subsequent cardiac remodeling.

Authors+Show Affiliations

Laboratory of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou 510080, People's Republic of China.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

17324585

Citation

Wang, Ping, et al. "Contribution of Different Nox Homologues to Cardiac Remodeling in Two-kidney Two-clip Renovascular Hypertensive Rats: Effect of Valsartan." Pharmacological Research, vol. 55, no. 5, 2007, pp. 408-17.
Wang P, Tang F, Li R, et al. Contribution of different Nox homologues to cardiac remodeling in two-kidney two-clip renovascular hypertensive rats: effect of valsartan. Pharmacol Res. 2007;55(5):408-17.
Wang, P., Tang, F., Li, R., Zhang, H., Chen, S., Liu, P., & Huang, H. (2007). Contribution of different Nox homologues to cardiac remodeling in two-kidney two-clip renovascular hypertensive rats: effect of valsartan. Pharmacological Research, 55(5), 408-17.
Wang P, et al. Contribution of Different Nox Homologues to Cardiac Remodeling in Two-kidney Two-clip Renovascular Hypertensive Rats: Effect of Valsartan. Pharmacol Res. 2007;55(5):408-17. PubMed PMID: 17324585.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Contribution of different Nox homologues to cardiac remodeling in two-kidney two-clip renovascular hypertensive rats: effect of valsartan. AU - Wang,Ping, AU - Tang,Futian, AU - Li,Ruifang, AU - Zhang,Huijie, AU - Chen,Shaorui, AU - Liu,Peiqing, AU - Huang,Heqing, Y1 - 2007/02/02/ PY - 2006/10/25/received PY - 2007/01/23/revised PY - 2007/01/26/accepted PY - 2007/2/28/pubmed PY - 2007/7/12/medline PY - 2007/2/28/entrez SP - 408 EP - 17 JF - Pharmacological research JO - Pharmacol Res VL - 55 IS - 5 N2 - Growing evidences have shown that hypertension, cardiac hypertrophy and fibrosis were associated with an overactivity of NAD(P)H oxidase. It is unknown, however, which isoform of NAD(P)H oxidase yields O(2)*(-) formation in heart and aorta in two-kidney, two-clip (2K2C) hypertensive rats in vivo and thus is responsible for the development of cardiac remodeling. We examined the pathological change of NAD(P)H oxidase homologues and tested the effect of valsartan on the cardiac remodeling in 2K2C renovascular hypertensive rats. Four weeks after male Sprague-Dawley rats accepted 2K2C or sham operation, 2K2C hypertensive (>160 mmHg) rats were divided into vehicle-treated (2K2C) and valsartan (30 mg kg(-1) per day, for 6 weeks)-treated (2K2C+Val) groups, which were compared with sham-operated controls (Sham). At week 10, 2K2C hypertensive rats showed increased serum level of angiotensin II (Ang II), MDA and blood pressure (BP), obvious cardiac hypertrophy and fibrosis, increased O(2)*(-) production and NAD(P)H oxidase activity and expression in aorta and heart. The heart in 2K2C hypertensive rats preferred to use NADH as substrate while the aorta used both NADH and NADPH. Valsartan treatment decreased BP, ameliorated cardiac hypertrophy and fibrosis, decreased O(2)*(-) production and NAD(P)H oxidase activity in aorta and heart. Nox2 and Nox4 protein expression increased in heart, while Nox1 and Nox4 increased in aorta in 2K2C hypertensive rats, which were all normalized after valsartan treatment. In conclusion, these data indicate that different Nox expression might account for substrate preference and the formation of O(2)*(-) by NAD(P)H oxidase resulting from elevated Ang II in the 2K2C model contributes to the development of renovascular hypertension and subsequent cardiac remodeling. SN - 1043-6618 UR - https://www.unboundmedicine.com/medline/citation/17324585/Contribution_of_different_Nox_homologues_to_cardiac_remodeling_in_two_kidney_two_clip_renovascular_hypertensive_rats:_effect_of_valsartan_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1043-6618(07)00040-0 DB - PRIME DP - Unbound Medicine ER -