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Cyclooxygenase-2 derived thromboxane A(2) and reactive oxygen species mediate flow-induced constrictions of venules

Anita Racz1, Zoltan Veresh, Gabor Lotz

  • 1Department of Pathophysiology, Semmelweis University, Budapest, Hungary.

Atherosclerosis
|July 21, 2009
PubMed

Insights

Hyperhomocysteinemia impairs venule function, causing flow-induced constrictions by increasing thromboxane A(2) and reactive oxygen species. This constricts blood vessels, potentially increasing vascular resistance and promoting thrombus formation.

Area of Science:

  • Vascular Biology
  • Cardiovascular Physiology
  • Endocrinology

Background:

  • Hyperhomocysteinemia (HHcy) is linked to arterial endothelial dysfunction and thrombosis.
  • The impact of HHcy on venular vasomotor function remains unstudied.

Purpose of the Study:

  • To investigate the effects of HHcy on the flow/shear stress-dependent vasomotor responses of venules.
  • To determine the underlying mechanisms of HHcy-induced changes in venular function.

Main Methods:

  • Isolated gracilis muscle venules from control and HHcy rats (methionine diet) were subjected to increased intraluminal flow.
  • Vessel diameter changes were measured, and the roles of thromboxane A(2) (TxA(2)) receptor, nitric oxide (NO) synthase, cyclooxygenase (COX) enzymes, and reactive oxygen species (ROS) were assessed using specific inhibitors and scavengers.

Main Results:

  • Increased flow caused dilation in control venules but constriction in HHcy venules.
  • Flow-induced constrictions in HHcy venules were reversed by a TxA(2) receptor antagonist and abolished by NO synthase and COX inhibitors.
  • COX-2 derived TxA(2) and ROS contributed to flow-induced constrictions, while COX-1 derived prostaglandins and NO had dilatory effects.

Conclusions:

  • HHcy induces flow-dependent venular constriction by increasing COX-2-derived TxA(2) and ROS production.
  • These mediators overcome NO and prostaglandin dilatory effects, increasing vascular resistance and promoting venular thrombus formation.
Abstract

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