Participation of Prostacyclin in Endothelial Dysfunction Induced by Aldosterone in Normotensive and Hypertensive Rats

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Abstract
The aim of the present study was to analyze the possible involvement of vasoconstrictors prostanoids on the reduced endothelium-dependent relaxations produced by chronic administration of aldosterone in Wistar Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). For this purpose, acetylcholine (ACh) relaxations in aortic segments from both strains were analyzed in absence and presence of the cyclooxygenase-1 (COX-1) and COX-2 inhibitor indomethacin, the specific COX-2 inhibitor NS-398, the TP receptor antagonist (SQ 29 548), the thromboxane A 2 (TXA 2 ) synthase inhibitor furegrelate, and the prostacyclin (PGI 2 ) synthesis inhibitor tranylcypromine (TCP). In addition, COX-2 protein expression was studied by Western blot analysis. Release of prostaglandin E 2 (PGE 2 ) and the metabolites of PGF 2α , TXA 2 , and PGI 2 , 13,14-dihydro-15-keto PGF 2a , TXB 2 , and 6-keto-PGF 1α , respectively, were measured. Treatment with aldosterone did not modify blood pressure levels in any strain. However, aldosterone markedly reduced ( P P 2a, PGE 2 , and 6-keto-PGF 1α ( P 1α production ( P 2 seems to be the main factor accounting for endothelial dysfunction in hypertensive rats, whereas other prostanoids besides PGI 2 appear to be involved in endothelial dysfunction under normotensive conditions.