Key result
Cyclooxygenase inhibitors potently reduce TxA2-receptor-mediated arterial contraction in mesenteric resistance vessels.
Why the study?
The role of cyclooxygenase pathway activation in thromboxane A2 receptor-dependent contraction in resistant arteries was not previously established.
Does cyclooxygenase pathway activation mediate thromboxane-dependent contraction in rat mesenteric resistance arteries?
Does cyclooxygenase pathway activation mediate thromboxane-dependent contraction in rat mesenteric resistance arteries?
Thromboxane A2-receptor-dependent contraction in resistance arteries involves cyclooxygenase stimulation and PGE2 formation, providing mechanistic insights relevant to diseases like hypertension.
Authors
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Does not yet alter clinical practice; leaves open the role of cyclooxygenase in human TxA2-dependent vasoconstriction.
Bolla et al. (2004) studied this question. Cyclooxygenase inhibitors (flurbiprofen, indomethacin, aspirin) vs. Control (U-46619 alone) was evaluated on U-46619-induced contraction (internal diameter reduction). Cyclooxygenase inhibitors potently reduced U-46619-induced contraction in rat mesenteric resistance arteries, demonstrating that TxA2-receptor-dependent contraction involves cyclooxygenase stimulation.