Overexpression of Arginase I Leads to Diminished Acetylcholine-Induced Coronary Arteriolar Dilation in Patients with Type 2 Diabetes Mellitus

Overexpression of Arginase I Leads to Diminished Acetylcholine-Induced Coronary Arteriolar Dilation in Patients with Type 2 Diabetes Mellitus

Bibliografiska uppgifter
Huvudupphovsmän:	Bagi, Z, Beleznai, T, Kaley, G
Materialtyp:	Conference item
Publicerad:	2009

Liknande verk

Arginase 1 contributes to diminished coronary arteriolar dilation in patients with diabetes.
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Upregulation of Arginase I Reduces Nitric Oxide-mediated Coronary Arteriolar Dilation in Patients With Type 2 Diabetes
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Transient elevation of glucose concentration reduces NO-mediation of flow-induced arteriolar dilation due to interaction between superoxide and tetrahydrobiopterin (BH4)
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Superoxide-NO interaction decreases flow- and agonist-induced dilations of coronary arterioles in Type 2 diabetes mellitus.
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Enhanced superoxide production reduces NO-mediation of flow-dependent dilation of isolated coronary arteries in type 2 diabetes mellitus
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Lack of nitric oxide mediation of flow-dependent arteriolar dilation in type I diabetes is restored by sepiapterin.
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Arginase promotes skeletal muscle arteriolar endothelial dysfunction in diabetic rats.
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H2O2 increases production of constrictor prostaglandins in smooth muscle leading to enhanced arteriolar tone in Type 2 diabetic mice.
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Obesity and statins are both independent predictors of enhanced coronary arteriolar dilation in patients undergoing heart surgery.
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Role of polyol pathway in oxidative stress-induced arteriolar dysfunction in diabetes mellitus (DM)
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Type 2 diabetic mice have increased blood pressure and enhanced arteriolar basal tone due to COX-2-dependent TxA(2)/PGH(2) production
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Xanthine oxidase-derived reactive oxygen species convert flow-induced arteriolar dilation to constriction in hyperhomocysteinemia: possible role of peroxynitrite.
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Obesity-induced reduction in nitric oxide-dependent arteriolar dilation in rats. Role of xanthine oxidase-derived superoxide.
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Selective Up-Regulation of Arginase 1 in Coronary Arteries of Diabetic Patients
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Peroxynitrite is responsible for flow-induced arteriolar constriction in hyperhomocysteinemia (HHcy)
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Asymmetrical dimethylarginine inhibits shear stress-induced nitric oxide release and dilation and elicits superoxide-mediated increase in arteriolar tone.
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Increased cyclooxygenase-2 expression and prostaglandin-mediated dilation in coronary arterioles of patients with diabetes mellitus.
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High-fat diet-induced reduction in nitric oxide-dependent arteriolar dilation in rats: role of xanthine oxidase-derived superoxide anion.
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Diabetes mellitus alters the intrinsic constrictor and dilator mechanisms regulating the tone of human coronary microvessels: Role of cyclooxygenase-2
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Hydrogen peroxide modulates arteriolar myogenic tone by activating multiple vasomotor mechanisms
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PPARgamma activation, by reducing oxidative stress, increases NO bioavailability in coronary arterioles of mice with Type 2 diabetes.
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O-Linked-n-Acetylglucosamine Formation Reduces Nitric Oxide-Dependent Dilation in Arterioles Exposed to High Glucose Concentrations
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Effect of arginase inhibition on ischemia-reperfusion injury in patients with coronary artery disease with and without diabetes mellitus.
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Reduced arteriolar smooth muscle responsiveness to nitric oxide in rats with mild uremia
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Specific roles of COX-1 and COX-2 inhibitors to interfere with the regulation of microvascular resistance in normal mice and mice with type 2 diabetes mellitus
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Oxidative stress via activating soluble guanylate cyclase leads to increased nitric oxide sensitivity of coronary arterioles in high fat diet-induced obesity
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High intraluminal pressure reduces AT1 receptor internalization and maintains arteriolar constrictions to angiotensin II
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Lingering Dynamics of Type 2 Diabetes Mellitus Red Blood Cells in Retinal Arteriolar Bifurcations
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Weekly doxorubicin increases coronary arteriolar wall and adventitial thickness.
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Biphasic effect of hydrogen peroxide on skeletal muscle arteriolar tone via activation of endothelial and smooth muscle signaling pathways.
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