Experimental Physiology Celebrating 100 years
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Physiology in Press

First published online on March 9, 2006.
Experimental Physiology (2006)
DOI: 10.1113/expphysiol.2005.033068
© The Physiological Society 2006
A more recent version of this article appeared on May 1, 2006
This Article
Right arrow Full Text (Rapid PDF)
Right arrow All Versions of this Article:
91/3/633    most recent
expphysiol.2005.033068v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hataishi, R.
Right arrow Articles by Scherrer-Crosbie, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hataishi, R.
Right arrow Articles by Scherrer-Crosbie, M.

Received December 13, 2005
Revised January 20, 2006
Accepted after revision March 6, 2006

Heart/Cardiac Muscle [240]

Nitric Oxide Synthase 2 and Pressure-Overload Induced Left Ventricular Remodeling in Mice

Ryuji Hataishi 1, Ana Clara Rodrigues 1, John G Morgan 1, Fumito Ichinose 1, Geneviève Derumeaux 1, Kenneth D Bloch 1, Michael H Picard 1, Marielle Scherrer-Crosbie 1*

1 Massachusetts General Hospital

* To whom correspondence should be addressed. E-mail: marielle{at}crosbie.com.


  Abstract
Nitric oxide synthase 2 (NOS2) has been reported to increase in hypertrophied cardiomyocytes, however whether nitric oxide synthase 2 (NOS2) plays a role in the development of hypertrophy is unknown. To investigate the relationship of NOS2 with LV remodeling 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 8 WT and 8 NOS2-/- were studied 42 days after TAC. Hemodynamic measurements were obtained before sacrifice. LV size and function was 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-/-. 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-/-. 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.

Key Words: Cardiovascular, Nitric oxide




This article has been cited by other articles:


Home page
 EndocrinologyHome page
X. Loyer, T. Damy, Z. Chvojkova, E. Robidel, F. Marotte, P. Oliviero, C. Heymes, and J.-L. Samuel
17{beta}-Estradiol Regulates Constitutive Nitric Oxide Synthase Expression Differentially in the Myocardium in Response to Pressure Overload
Endocrinology, October 1, 2007; 148(10): 4579 - 4584.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
H. Thibault, L. Gomez, E. Donal, G. Pontier, M. Scherrer-Crosbie, M. Ovize, and G. Derumeaux
Acute myocardial infarction in mice: assessment of transmurality by strain rate imaging
Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H496 - H502.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2006 by the The Physiological Society.