Abstract

The effects of the arachidonic acid metabolism inhibitors on the acetylcholine responses of aortae from control (CR) and deoxycorticosterone acetate (DOCA)-salt hypertensive (HR) rats were investigated. The acetylcholine decreased response observed in HR relaxation % : CR 95.5 ± 2.7, n = 4; HR 52.0 ± 6.3, n = 5, p < 0.05 was restored by the cyclooxygenase inhibitor piroxicam relaxation % : CR 99.8 ± 0.2, n = 4; HR 86.0 ± 4.0, n = 5 and by the thromboxane synthetase inhibitor and the thromboxane A 2/prostaglandin H 2 receptor antagonist ridogrel relaxation % : CR 92.1 ± 4.4, n = 7; HR 93.1 ± 2.0, n = 7 but not by the inhibitors of thromboxane synthetase, prostacyclin synthetase, cytochrome P-450 monooxygenase, and lipoxygenase. So, endoperoxide intermediates seem to be involved in the decreased endothelium-dependent relaxation to acetylcholine in DOCA-salt hypertension.

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