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Enhanced Peroxynitrite Formation Is Associated with Vascular Aging
TLDR
Lower free nitric oxide levels in aged rat aortas are found in conjunction with a sevenfold higher expression and activity of endothelial NO synthase (eNOS), which suggests that mitochondrial dysfunction plays a major role in the vascular aging process. Expand
Central role of mitochondrial aldehyde dehydrogenase and reactive oxygen species in nitroglycerin tolerance and cross-tolerance.
TLDR
Nitrate tolerance is mediated, at least in significant part, by inhibition of vascular ALDH-2 and that mitochondrial ROS contribute to this inhibition, and GTN tolerance may be viewed as a metabolic syndrome characterized by mitochondrial dysfunction. Expand
High Glucose Causes Upregulation of Cyclooxygenase-2 and Alters Prostanoid Profile in Human Endothelial Cells: Role of Protein Kinase C and Reactive Oxygen Species
TLDR
High glucose, via PKC signaling, induces oxidative stress and upregulation of COX-2, resulting in reduced NO availability and altered prostanoid profile. Expand
Inhibition of platelet aggregation by carbon monoxide is mediated by activation of guanylate cyclase.
TLDR
It is concluded that cGMP is an important feedback regulator of the Pl response and that already a 25% increase in its steady state levels can cause inhibition of platelet aggregation. Expand
Vascular Consequences of Endothelial Nitric Oxide Synthase Uncoupling for the Activity and Expression of the Soluble Guanylyl Cyclase and the cGMP-Dependent Protein Kinase
TLDR
The present review summarizes current concepts concerning eNOS uncoupling and also focuses on the consequences for downstream signaling with respect to activity and expression of the sGC and cGK-I in various diseases. Expand
Peroxynitrite and vascular endothelial dysfunction in diabetes mellitus.
TLDR
The authors' studies indicate that in diabetes the synthetic enzymes of the two major endogenous vasodilators undergo oxidative inactivation by different mechanisms, which are, however, tightly interdependent. Expand
Peroxynitrite formed by simultaneous generation of nitric oxide and superoxide selectively inhibits bovine aortic prostacyclin synthase
TLDR
Peroxynitrite irreversibly blocked prostacyclin biosynthesis with an IC50 value of 50 nM, suggesting that under pathological conditions like ischemia‐reperfusion not only the vasodilatory effects of nitric oxide but also those of prostacyClin could be eliminated. Expand
Tyrosine Nitration as a Mechanism of Selective Inactivation of Prostacyclin Synthase by Peroxynitrite
TLDR
The simultaneous generation of superoxide and nitric oxide proved to be as efficient as a bolus of peroxynitrite which supports a possible inactivation of prostacyclin synthase under in vivo conditions, and substantiates an often suggested crucial role ofsuperoxide in the pathophysiology of the cardiovascular system. Expand
On the mechanism of prostacyclin and thromboxane A2 biosynthesis.
TLDR
A cage radical mechanism is proposed for both enzymes according to which the initial radical process is terminated through oxidation of carbon-centered radicals by the iron-sulfur catalytic site, followed by ionic rearrangement to PGI2 or TXA2. Expand
Molecular cloning and expression of human prostacyclin synthase.
TLDR
Tissue distribution study demonstrated that prostacyclin synthase mRNA is widely expressed in human tissues and is particularly abundant in ovary, heart, skeletal muscle, lung, and prostate, suggesting a variety of physiological roles of prostacyClin in addition to the implications in the cardiovascular system. Expand
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