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Pressure overload-induced LV hypertrophy and dysfunction in mice are exacerbated by congenital NOS3 deficiency
- Source :
- American journal of physiology. Heart and circulatory physiology. 286(3)
- Publication Year :
- 2003
-
Abstract
- To investigate the role of endothelial nitric oxide synthase (NOS3) in left ventricular (LV) remodeling induced by chronic pressure overload, the impact of transverse aortic constriction (TAC) on LV structure and function was compared in wild-type (WT) and NOS3-deficient (NOS3–/–) mice. Before TAC, LV wall thickness, mass, and fractional shortening were similar in the two mouse strains. Twenty-eight days after TAC, both WT and NOS3–/– mice had increased LV wall thickness and mass as well as decreased fractional shortening. Although the pressure gradient across the TAC was similar in both strains of mice 28 days after TAC, LV mass and posterior wall thickness were greater in NOS3–/– than in WT mice, whereas fractional shortening and the maximum rate of developed LV pressure were less. Diastolic function, as measured by the time constant of isovolumic relaxation and the maximum rate of LV pressure decay, was impaired to a greater extent in NOS3–/– than in WT mice. The degree of myocyte hypertrophy and LV fibrosis was greater in NOS3–/– than in WT mice at 28 days after TAC. Mortality was greater in NOS3–/– than in WT mice 28 days after TAC. Long-term administration of hydralazine normalized the blood pressure and prevented the LV dilation in NOS3–/– mice but did not prevent the LV hypertrophy, dysfunction, and fibrosis associated with NOS3 deficiency after TAC. These results suggest that the absence of NOS3 augments LV dysfunction and remodeling in a murine model of chronic pressure overload.
- Subjects :
- Male
medicine.medical_specialty
Heart disease
Nitric Oxide Synthase Type III
Physiology
Nitric Oxide Synthase Type II
Muscle hypertrophy
Mice
Ventricular Dysfunction, Left
Fibrosis
Physiology (medical)
Internal medicine
medicine
Myocyte
Animals
Myocytes, Cardiac
cardiovascular diseases
Aorta
Pressure overload
business.industry
Organ Size
medicine.disease
Mice, Mutant Strains
body regions
Mice, Inbred C57BL
Survival Rate
Disease Models, Animal
Endocrinology
Echocardiography
Heart failure
Circulatory system
cardiovascular system
Hypertrophy, Left Ventricular
Nitric Oxide Synthase
Cardiology and Cardiovascular Medicine
business
Subjects
Details
- ISSN :
- 03636135
- Volume :
- 286
- Issue :
- 3
- Database :
- OpenAIRE
- Journal :
- American journal of physiology. Heart and circulatory physiology
- Accession number :
- edsair.doi.dedup.....2ca8967af6b2571e83cfec5c25a16d89