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CONSTITUTIVE NITRIC OXIDE SYNTHASES IN THE HEART FROM HYPERTROPHY TO FAILURE
Author(s) -
Loyer Xavier,
Heymes Christophe,
Samuel JaneLise
Publication year - 2008
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2008.04901.x
Subject(s) - nos1 , nitric oxide , heart failure , pressure overload , nitric oxide synthase , muscle hypertrophy , medicine , myocardial infarction , cardiology , biology , microbiology and biotechnology , endocrinology , cardiac hypertrophy
SUMMARY1 Endogenous myocardial nitric oxide (NO) may modulate the transition from adaptive to maladaptive hypertrophy leading to heart failure. This review summarizes the information on the interrelations between the precise localization of NO synthases (NOS) and their regulatory functions within different compartments of the heart. 2 In rodent models of pressure overload or myocardial infarction, the three NOS isoforms (NOS1, NOS2, NOS3) were shown to play a neutral, protective, or even adverse role in myocardial remodelling, depending on the NOS activity, the location of each NOS and their regulators. 3 The analysis of conditions that modulate the expression of NOS1 and NOS3 in the heart according to physiopathological situations, indicated that, beside the level of total NOS activity, unique changes in NO compartmentation secondary to NOS1 or NOS3 subcellular location might be involved in the development of cardiac hypertrophy and failure. 4 Thus, different circuits in NO‐signalling pathways in myocardium might be activated and this principle is a key to understand contradictions existing in NO biology in the heart. Unravelling the mechanisms behind the NO, NOS and cardiac function is still an ongoing challenge.