Faculty Collaboration Database

Ablation of iNOS delays cardiac contractile dysfunction in chronic hypertension. Front Biosci (Elite Ed) 2010 Jan 01;2(1):312-24

Date

12/29/2009

Pubmed ID

20036880

Pubmed Central ID

PMC2901916

DOI

10.2741/e92

Scopus ID

2-s2.0-77954525347 (requires institutional sign-in at Scopus site)   23 Citations

Abstract

We investigated the role of inducible NOS (iNOS) on cardiac function during the development of left ventricular hypertrophy. Hypertrophy was induced by pressure-overload via short-term (2.5 months) or long-term (6.5 months) aortic banding (AoB) in wild-type (WT) and iNOS knock out (iNOSKO) mice. Cardiac function was then assessed via echocardiography, in situ hemodynamics and papillary muscle force measurements. Quantitative RT-PCR and Western blots were used to measure expression of hypertrophic gene markers and proteins respectively. Our data demonstrate that increased afterload via AoB leads to increased expression of iNOS that is associated with cardiac dysfunction. In pressure-overload induced hypertrophy, iNOSKO delays both the expression of hypertrophic markers and contractile dysfunction without causing significant changes in the level of hypertrophy. Moreover, after long-term AoB, iNOSKO animals exhibited increased basal cardiac function and an improved response to beta-adrenergic stimulation compared to long-term AoB WT animals. In conclusion, our data demonstrate that NO production via iNOS plays an important role in modulating cardiac function after moderate AoB that mimics long-term hypertension in humans.

Author List

Dias FA, Urboniene D, Yuzhakova MA, Biesiadecki BJ, Pena JR, Goldspink PH, Geenen DL, Wolska BM

MESH terms used to index this publication - Major topics in bold

Analysis of Variance
Animals
Aorta
Biomarkers
Blotting, Western
Echocardiography
Fluorescent Antibody Technique
Hemodynamics
Hypertension
Hypertrophy, Left Ventricular
Ligation
Male
Mice
Myocardial Contraction
Myosin Heavy Chains
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Papillary Muscles
Reverse Transcriptase Polymerase Chain Reaction