Nitric oxide synthase 2 and pressure-overload-induced left ventricular remodelling in mice

Experimental Physiology
Ryuji HataishiM Scherrer-Crosbie

Abstract

Nitric oxide synthase 2 (NOS2) has been reported to increase in hypertrophied cardiomyocytes; however, whether NOS2 plays a role in the development of hypertrophy is unknown. To investigate the relationship of NOS2 with left ventricular (LV) remodelling and hypertrophy following prolonged pressure overload, we studied 18 male wild-type (WT) and 20 male NOS2-deficient (NOS2-/-) mice before and 7, 14 and 28 days after transverse aortic constriction (TAC) using echocardiography. A subgroup of eight WT and eight NOS2-/- mice were studied 42 days after TAC. Haemodynamic measurements were obtained before killing. Left ventricular size and function were similar for both genotypes at baseline. After TAC for 28 days, both groups developed LV hypertrophy, with echo-derived LV mass increasing from 78 +/- 2 to 147 +/- 10 mg in WT and from 86 +/- 3 to 142 +/- 10 mg in NOS2-/- mice. Twenty-eight days after TAC, LV weight and cardiomyocyte width were also similar in both genotypes. Fractional shortening (FS) decreased on day 7 from 57 +/- 1 to 48 +/- 2% in WT and from 59 +/- 1 to 49 +/- 2% in NOS2-/- mice. Although this decrease in FS was transient in WT mice, it persisted in NOS2-/- mice. Invasively measured parameters of systolic and diasto...Continue Reading

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Citations

Mar 28, 2007·Current Heart Failure Reports·Paul B Massion, Jean-Luc Balligand
Jan 10, 2012·Cardiovascular Research·Boris ManouryJean-Luc Balligand
Jul 21, 2009·Journal of Molecular and Cellular Cardiology·Marielle Scherrer-Crosbie, Baptiste Kurtz
Aug 17, 2011·Journal of Molecular and Cellular Cardiology·Joanna Hammond, Jean-Luc Balligand
Mar 27, 2007·American Journal of Physiology. Heart and Circulatory Physiology·Hélène ThibaultGeneviève Derumeaux

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