15 research outputs found
Cytokines Increase Neonatal Cardiac Myocyte Calcium Concentrations: The Involvement of Nitric Oxide and Cyclic Nucleotides
Real-time RT-PCR for the Detection of Beta-adrenoceptor Messenger RNAs in Small Human Endomyocardial Biopsies
Enhanced ?-adrenergic response in rat papillary muscle by inhibition of inducible nitric oxide synthase after myocardial infarction
Reference Models for Mitral Valve Tissue Engineering Based on Valve Cell Phenotype and Extracellular Matrix Analysis
Interaction between Hydrogen Sulfide and Muscarinic Receptors in the Regulation of Contractility of the Mouse Atrium
Relevance of nitric oxide for myocardial remodeling.
Endogenous myocardial nitric oxide (NO) may modulate the transition from adaptive to maladaptive remodeling leading to heart failure. In rodent models of pressure overload or myocardial infarction, the three NO synthase (NOS) isoforms were shown to play a neutral, protective, or even adverse role in myocardial remodeling, depending on the quantity of NO produced, the location of each NOS and their regulators, the prevailing oxidant stress and resultant NO/oxidant balance, as well as NOS coupling/dimerization. Beside neuronal NOS and--in specific conditions--inducible NOS isoforms, endothelial NOS (eNOS) exerts cardioprotective effects on pressure-overload, ischemia/reperfusion, and myocardial infarction-induced myocardial remodeling, provided the enzyme remains in a coupled state. Besides its effects on excitation-contraction coupling in response to stretch, eNOS acts as an "endogenous beta-blocker" by restoring the sympathovagal balance, opposing excessive hypertrophy as well as promoting vasodilatation and neoangiogenesis, thereby contributing to tissue repair. As eNOS was also shown to mediate the beneficial effects of cardiovascular drugs commonly used in patients with heart failure, strategies to increase its expression and/or coupled catalytic activity in the myocardium offer new therapeutic avenues for the treatment of this disease