Thromboxane A2 contributes to the mediation of flow-induced responses of skeletal muscle venules: Role of cyclooxygenases 1 and 2

A. Racz, Z. Veresh, N. Erdei, Z. Bagi, A. Koller

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Background: It has been shown that increases in intraluminal flow elicit dilation in venules, but the mediation of response is not yet clarified. We hypothesized that - in addition to nitric oxide (NO) and dilator prostaglandins (PGI2/ PGE2) - thromboxane A2 (TxA2) contributes to the mediation of flow-induced responses of venules. Methods and Results: Isolated rat gracilis muscle venules (259 ± 11 μm at 10 mm Hg) dilated as a function of intraluminal flow, which was augmented in the presence of the TxA2 receptor antagonist SQ 29,548 or the TxA 2 synthase inhibitor ozagrel. In the presence of SQ 29,548, indomethacin or Nω-nitro-L-arginine methyl-ester decreased flow-induced dilations, whereas in their simultaneous presence dilations were abolished. The selective cyclooxygenase (COX) 1 inhibitor SC 560 reduced, whereas the selective COX-2 inhibitor NS 398 enhanced flow-induced dilations. Immunohistochemistry showed that both COX-1 and COX-2 are present in the wall of venules. Conclusion: In skeletal muscle venules, increases in intraluminal flow elicit production of constrictor TxA2, in addition to the dilator NO and PGI 2/PGE2, with an overall effect of limited dilation. These mediators are likely to have important roles in the multiple feedback regulation of wall shear stress in venules during changes in blood flow velocity and/or viscosity.

Original languageEnglish (US)
Pages (from-to)397-405
Number of pages9
JournalJournal of Vascular Research
Volume46
Issue number5
DOIs
StatePublished - Aug 1 2009

Fingerprint

Cyclooxygenase 1
Thromboxane A2
Venules
Cyclooxygenase 2
Skeletal Muscle
Dilatation
Dinoprostone
Nitric Oxide
Prostaglandin H2 Receptors Thromboxane A2
Cyclooxygenase Inhibitors
Blood Flow Velocity
Cyclooxygenase 2 Inhibitors
Epoprostenol
Viscosity
Indomethacin
Prostaglandins
Immunohistochemistry

Keywords

  • Cyclooxygenases 1 and 2
  • Nitric oxide
  • Prostaglandins
  • Shear stress
  • Thromboxane A synthase
  • Venule

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Thromboxane A2 contributes to the mediation of flow-induced responses of skeletal muscle venules : Role of cyclooxygenases 1 and 2. / Racz, A.; Veresh, Z.; Erdei, N.; Bagi, Z.; Koller, A.

In: Journal of Vascular Research, Vol. 46, No. 5, 01.08.2009, p. 397-405.

Research output: Contribution to journalArticle

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abstract = "Background: It has been shown that increases in intraluminal flow elicit dilation in venules, but the mediation of response is not yet clarified. We hypothesized that - in addition to nitric oxide (NO) and dilator prostaglandins (PGI2/ PGE2) - thromboxane A2 (TxA2) contributes to the mediation of flow-induced responses of venules. Methods and Results: Isolated rat gracilis muscle venules (259 ± 11 μm at 10 mm Hg) dilated as a function of intraluminal flow, which was augmented in the presence of the TxA2 receptor antagonist SQ 29,548 or the TxA 2 synthase inhibitor ozagrel. In the presence of SQ 29,548, indomethacin or Nω-nitro-L-arginine methyl-ester decreased flow-induced dilations, whereas in their simultaneous presence dilations were abolished. The selective cyclooxygenase (COX) 1 inhibitor SC 560 reduced, whereas the selective COX-2 inhibitor NS 398 enhanced flow-induced dilations. Immunohistochemistry showed that both COX-1 and COX-2 are present in the wall of venules. Conclusion: In skeletal muscle venules, increases in intraluminal flow elicit production of constrictor TxA2, in addition to the dilator NO and PGI 2/PGE2, with an overall effect of limited dilation. These mediators are likely to have important roles in the multiple feedback regulation of wall shear stress in venules during changes in blood flow velocity and/or viscosity.",
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AB - Background: It has been shown that increases in intraluminal flow elicit dilation in venules, but the mediation of response is not yet clarified. We hypothesized that - in addition to nitric oxide (NO) and dilator prostaglandins (PGI2/ PGE2) - thromboxane A2 (TxA2) contributes to the mediation of flow-induced responses of venules. Methods and Results: Isolated rat gracilis muscle venules (259 ± 11 μm at 10 mm Hg) dilated as a function of intraluminal flow, which was augmented in the presence of the TxA2 receptor antagonist SQ 29,548 or the TxA 2 synthase inhibitor ozagrel. In the presence of SQ 29,548, indomethacin or Nω-nitro-L-arginine methyl-ester decreased flow-induced dilations, whereas in their simultaneous presence dilations were abolished. The selective cyclooxygenase (COX) 1 inhibitor SC 560 reduced, whereas the selective COX-2 inhibitor NS 398 enhanced flow-induced dilations. Immunohistochemistry showed that both COX-1 and COX-2 are present in the wall of venules. Conclusion: In skeletal muscle venules, increases in intraluminal flow elicit production of constrictor TxA2, in addition to the dilator NO and PGI 2/PGE2, with an overall effect of limited dilation. These mediators are likely to have important roles in the multiple feedback regulation of wall shear stress in venules during changes in blood flow velocity and/or viscosity.

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