Key result
NOS2 deficiency did not significantly alter left ventricular hypertrophy after 28 days of pressure overload, with LV mass reaching 142 mg in NOS2-deficient versus 147 mg in wild-type mice.
Why the study?
Does NOS2 deficiency affect left ventricular remodeling and hypertrophy following prolonged pressure overload in mice?
Does NOS2 deficiency affect left ventricular remodeling and hypertrophy following prolonged pressure overload in mice?
Absolute Event Rate: 142% vs 147%
NOS2 does not appear to play a critical role in the development of left ventricular hypertrophy after chronic pressure overload in mice.
Does not support NOS2 as a target to limit pressure-overload LVH; leaves open isoform or species differences in remodeling.
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 diastolic function, however, were similar in the two genotypes both 28 and 42 days after TAC. A load-independent index of contractility, Emax, was similar in both strains 42 days after TAC. In conclusion, NOS2 does not appear to have a critical role in the development of LV hypertrophy after chronic pressure overload.
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Hataishi et al. (2006) studied Left ventricular remodelling and hypertrophy (n=38). NOS2 deficiency vs. Wild-type was evaluated on Left ventricular mass at 28 days. NOS2 deficiency did not significantly alter left ventricular hypertrophy after 28 days of pressure overload, with LV mass reaching 142 mg in NOS2-deficient versus 147 mg in wild-type mice.
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