Intrinsic vascular mechanisms stimulated by changes in pressure and now elicit reactive dilatation of isolated arterioles

Intrinsic vascular mechanisms stimulated by changes in pressure and now elicit reactive dilatation of isolated arterioles

Sonraí bibleagrafaíochta
Príomhchruthaitheoirí:	Bagi, Z, Ungvari, Z, Koller, A
Formáid:	Journal article
Foilsithe / Cruthaithe:	2000

Míreanna comhchosúla

Nitric oxide and hydrogen peroxide contribute to the development of reactive dilation in isolated coronary arterioles
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Nitric oxide and H2O2 contribute to reactive dilation of isolated coronary arterioles.
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Impaired flow-induced dilation in skeletal muscle arterioles of rats with hyperhomocysteinemia (HHCY). Role of nitric oxide and constrictor prostanoids.
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Tetrahydrobiopterin (BH4) is essential for NO-mediated flow-dependent dilation of isolated skeletal muscle arterioles
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Simultaneously increased TxA(2) activity in isolated arterioles and platelets of rats with hyperhomocysteinemia.
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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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Xanthine oxidase-derived reactive oxygen species convert flow-induced arteriolar dilation to constriction in hyperhomocysteinemia. Possible role of peroxynitrite
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Increased PGH(2)/TXA(2) synthesis in isolated arterioles and platelets of rats with hyperhomocysteinemia (HHCY).
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PPAR gamma activation restores NO-Mediated dilations of coronary Arterioles in type 2 diabetes Mellitus
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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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High intraluminal pressure reduces tachyphylaxis to angiotensin II in isolated arterioles
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Chronic renal failure leads to reduced flow-dependent dilation in isolated rat skeletal muscle arterioles due to lack of NO mediation.
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On the role of mechanosensitive mechanisms eliciting reactive hyperemia.
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PECAM-1 mediates NO-dependent dilation of arterioles to high temporal gradients of shear stress.
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Flow-induced constriction in arterioles of hyperhomocysteinemic rats is due to impaired nitric oxide and enhanced thromboxane A(2) mediation.
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Increased activity of tissue ACE impairs dilation of coronary arterioles in obesity
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Increased cyclooxygenase-2 expression and prostaglandin-mediated dilation in coronary arterioles of patients with diabetes mellitus.
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Lack of flow-mediated dilation and enhanced angiotensin II-induced constriction in skeletal muscle arterioles of lupus-prone autoimmune mice.
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The levosimendan metabolite OR-1896 elicits vasodilation by activating the K(ATP) and BK(Ca) channels in rat isolated arterioles.
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The levosimendan metabolite OR-1896 elicits vasodilation by activating the K(ATP) and BK(Ca) channels in rat isolated arterioles.
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Functional and morphological evidence for increased peroxynitrite formation in hyperhomocysteinemia impairing flow-induced coronary dilation
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Hydrogen peroxide elicits COX-2-dependent production of constrictor prostaglandins in arterioles of type 2 diabetic mice
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Impaired nitric oxide-mediated flow-induced coronary dilation in hyperhomocysteinemia: morphological and functional evidence for increased peroxynitrite formation.
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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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Multiple effects of diabetes mellitus on the vasomotor responses of human coronary arterioles
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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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PPARgamma activation, by reducing oxidative stress, increases NO bioavailability in coronary arterioles of mice with Type 2 diabetes.
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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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Asymmetrical dimethylarginine inhibits shear stress-induced nitric oxide release and dilation and elicits superoxide-mediated increase in arteriolar tone.
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Conducted dilatation to ATP and K+ in rat skeletal muscle arterioles
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Conducted vasodilatation in human coronary arterioles
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Impaired NO-mediation of flow dependent arteriolar dilation in diabetes due to reduced level of tetrahydrobiopterin
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Aldose reductase inhibition reduces endothelial dysfunction and oxidative stress in skeletal muscle arterioles exposed to hyperglycemia
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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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Role of platelet endothelial adhesion molecule (PECAM)-1 in sensing and mediating high temporal gradients of shear stress in arterioles
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Adaptation of vasomotor function of human coronary arterioles to the simultaneous presence of obesity and hypertension.
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Asymmetric dimethylarginine (ADMA) increases the myogenic tone of arterioles due to enhanced release of superoxide
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Preserved coronary arteriolar dilatation in patients with type 2 diabetes mellitus: implications for reactive oxygen species.
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Increased soluble guanylate cyclase (sGC) activity may compensate for the high fat diet-induced reduction in NO bioavailability of rat coronary arterioles
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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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