Key result
The contractile effect of NO synthase blockade in isolated rat middle cerebral arteries was markedly attenuated by cyclooxygenase or thromboxane A2 inhibition.
Inhibition of NO synthesis induces vasoconstriction in rat cerebral arteries partly through the release of thromboxane A2.
Suggests TxA2 mediation of cerebral vasoconstriction after NO blockade in rats; leaves open translation to human vasoregulation.
Inhibition of nitric oxide (NO) synthesis induces vasoconstriction and reduction of the blood flow in the brain, indicating that basal release of NO provides a resting vasorelaxant tone in the cerebral circulation. In the present study, the contractile effect of the NO synthase blocker NG-nitro-L-arginine (100 mumol/L) in isolated rat middle cerebral arteries was attenuated markedly in the presence of the cyclooxygenase inhibitor indomethacin (5 mumol/L), the thromboxane A2 synthase inhibitor ridogrel (10 mumol/L), or the thromboxane receptor antagonist ICI 192605 (100 mumol/L). These results indicate that removal of the endogenous NO stimulates the release of thromboxane A2 in cerebral vessels and basal NO production regulates the resting cerebrovascular tone, at least in part, by suppressing thromboxane A2.
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Benyó et al. (1998) studied Isolated rat middle cerebral arteries. Cyclooxygenase or thromboxane A2 inhibitors (indomethacin, ridogrel, or ICI 192605) vs. NO synthase blocker NG-nitro-L-arginine (100 mumol/L) alone was evaluated on Contractile effect. The contractile effect of NO synthase blockade in isolated rat middle cerebral arteries was markedly attenuated by cyclooxygenase or thromboxane A2 inhibition.
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