By Joseph Loscalzo, Joseph A. Vita
Top medical and experimental investigators comprehensively evaluate the chemistry, biochemistry, molecular biology, body structure, and pathophysiology of nitric oxide within the cardiovascular platforms. those specialists fairly remove darkness from nitric oxide biology, its cardiovascular pathophysiology, and its function in cardiovascular therapeutics. subject matters additionally integrated are the advance of nitric oxide donors for the remedy of myocardial ischemia and thrombosis, the advance of gene healing recovery of endothelial functionality in atherosclerosis, and the appliance of nitric oxide biology to investigative arenas in cardiovascular drugs. With its balanced presentation of uncomplicated and clinically proper info, Nitric Oxide and the Cardiovascular method offers a entire, authoritative advisor for all these cardiovascular biologists, cardiologists, physiologists, and cardiovascular surgeons engaged in state-of-the-art scientific or experimental learn.
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Extra resources for Nitric Oxide and the Cardiovascular System (Contemporary Cardiology) (Contemporary Cardiology)
Biochem J 1996;314:889–894. 88. Michel T, Li GK, Busconi L. Phosphorylation and subcellular translocation of endothelial nitric oxide synthase. Proc Natl Acad Sci USA 1993;90:6252–6256. 89. Tsukahara H, Gordienko DV, Goligorsky MS. Continuous monitoring of nitric oxide release from human umbilical vein endothelial cells. Biochem Biophys Res Commun 1993;193:722–729. 90. Craven PA, Studer RK, DeRubertis FR. Impaired nitric oxide-dependent cyclic guanosine monophosphate generation in glomeruli from diabetic rats.
In the specific case of shear stress, the eNOS/Hsp90 association appears to be somewhat delayed relative to that seen following agonist stimulation (94) and may correspond with the slower change in detergent solubility of eNOS seen in endothelial cells following exposure to shear stress (93). 24 Part I / Biology of Nitric Oxide Caveolin-1, Caveolin-3 and Their Regulatory Cycles Following the original observation of the caveolar localization of eNOS in plasmalemmal caveolae (96), several lines of evidence in endothelial cells and cardiac myocytes revealed that eNOS is quantitatively associated with caveolin, the structural protein within caveolae (141).
Interestingly, enhanced production of peroxynitrite can lead to inactivation of the sarcolemma calcium ATPase via tyrosine nitration in exhaustively exercised skeletal muscle (6). Because high levels of peroxynitrite are also associated with atherosclerotic plaque formation, this phenomenon may prove to be relevant to vascular responses in atherothrombosis. In contrast, L-type voltage-dependent calcium channels, which permit the inward flow of calcium when cells become depolarized, are inhibited by NO• by what is apparently a PKG-independent mechanism.