Cyclooxygenase-dependent vasoconstrictor alters vascular function in the vitamin E-deprived rat

Area of Science:

• Vascular Biology
• Nutritional Biochemistry
• Pharmacology

Background:

• Dietary vitamin E deprivation is known to increase lipid peroxidation.
• Lipid peroxidation can impact cellular function and signaling pathways.
• The cyclooxygenase pathway plays a critical role in vascular tone regulation.

Purpose of the Study:

• To investigate the effect of vitamin E deprivation-induced lipid peroxidation on vascular function.
• To determine if the cyclooxygenase pathway is altered in vitamin E-deprived rats.
• To examine the role of thromboxane A2/prostaglandin H2 receptor in these vascular changes.

Main Methods:

• Mesenteric arteries from control and vitamin E-deprived Sprague-Dawley rats were studied using myography.
• Endothelium-dependent and independent relaxations were assessed.
• The effects of cyclooxygenase and thromboxane A2/prostaglandin H2 receptor inhibitors were evaluated.
• Arachidonic acid-induced tension and prostaglandin endoperoxide synthase expression were measured.

Main Results:

• Vitamin E deprivation did not alter basal endothelium-dependent relaxations but potentiated them in the presence of inhibitors.
• Arachidonic acid caused greater vasoconstriction in vitamin E-deprived rats, an effect blunted by inhibitors.
• Prostaglandin endoperoxide synthase expression was increased in vitamin E-deprived rats.
• Endothelium-independent relaxations were unaffected.

Conclusions:

• Vitamin E-deprived rats exhibit altered endothelium-dependent vascular responses.
• These alterations are partly mediated by a cyclooxygenase-dependent vasoconstrictor acting on the thromboxane A2/prostaglandin H2 receptor.
• Increased lipid peroxidation may influence vascular function in disease states by modulating the cyclooxygenase pathway.