The role of cycloxygenase-1 and-2 (COX-1,-2) in mediation of flow-induced responses of venules

The role of cycloxygenase-1 and-2 (COX-1,-2) in mediation of flow-induced responses of venules

Bibliografski detalji
Glavni autori:	Racz, A, Veresh, Z, Erdei, N, Bagi, Z, Koller, A
Format:	Journal article
Izdano:	2009

Slični predmeti

Thromboxane A(2) contributes to the mediation of flow-induced responses of skeletal muscle venules: role of cyclooxygenases 1 and 2.
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Cyclooxygenase-2 derived thromboxane A(2) and reactive oxygen species mediate flow-induced constrictions of venules in hyperhomocysteinemia.
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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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High intraluminal pressure via H2O2 upregulates arteriolar constrictions to angiotensin II by increasing the functional availability of AT1 receptors.
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Type 2 diabetic mice have increased arteriolar tone and blood pressure: enhanced release of COX-2-derived constrictor prostaglandins.
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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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Flow-induced constriction in arterioles of hyperhomocysteinemic rats is due to impaired nitric oxide and enhanced thromboxane A(2) mediation.
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Peroxynitrite is responsible for flow-induced arteriolar constriction in hyperhomocysteinemia (HHcy)
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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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H2O2 increases production of constrictor prostaglandins in smooth muscle leading to enhanced arteriolar tone in Type 2 diabetic mice.
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Tetrahydrobiopterin (BH4) is essential for NO-mediated flow-dependent dilation of isolated skeletal muscle arterioles
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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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Lack of nitric oxide mediation of flow-dependent arteriolar dilation in type I diabetes is restored by sepiapterin.
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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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Impaired flow-induced dilation in skeletal muscle arterioles of rats with hyperhomocysteinemia (HHCY). Role of nitric oxide and constrictor prostanoids.
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