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Endothelial dysfunction in DOCA-salt hypertension: possible involvement of prostaglandin endoperoxides
1Department of Pharmacology, Institute of Biosciences, University Estadual Paulista, São Paulo, Brazil. cordelli@ibb.unesp.br
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 A2/prostaglandin H2 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.