Abstract
Cyclooxygenase-2 inhibition causes an increase of norepinephrine vasoconstriction. The aim of this study is to evaluate the role of increased prostaglandins (PG) E2/I2 on the vascular reactivity to norepinephrine under inflammatory conditions. Using organ bath experiments, the contraction induced by norepinephrine was studied on isolated human internal mammary arteries cultured for 24h in the presence or absence of both interleukin-1β and lipopolysaccharide. The expression of PG receptors and PG synthases was detected by immunohistochemistry. Contractions induced by norepinephrine in arteries submitted to inflammatory conditions, were significantly increased (55±18%, n=6, P<0.05) after treatment with the PGI2 receptor antagonist, CAY 10441, whereas no difference in reactivity was observed in presence of PGE2 receptor antagonists. Under these conditions, the expression of PG receptors and synthases was not modified. These results demonstrate that under inflammatory conditions, PGI2, but not PGE2, is responsible for the increase in vascular tone after cyclooxygenase-2 inhibition.
Published Version
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