Effects of 17β-oestradiol on rat isolated coronary and mesenteric artery tone: Involvement of nitric oxide

Pre- and post-menopausal women receiving oestrogen replacement therapy have a significantly reduced risk of cardiovascular disorders. It has been suggested that this protection might be partly a result of a direct relaxant effect of oestrogens on coronary arteries. This study examines and directly compares the effects of 17β-oestradiol on rat isolated coronary and mesenteric vessels. The influence of nitric oxide on these responses was also investigated. 17β-Oestradiol caused similar concentration-dependent relaxation of isolated coronary and mesenteric resistance arteries pre-contracted with either KCl (60 mM) or 9,11-dideoxy-11α,9α-epoxymethanoprostaglandin (U46619; 1 μM). The relaxation responses to 17β-oestradiol were significantly reduced, but not totally inhibited, in the presence of N(ω)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase; they were not altered by indomethacin, an inhibitor of prostaglandin synthesis. The responses to 17β-oestradiol in the presence of L-NAME were not dependent on the vessel studied or the precontracting agent used. These results suggest that nitric oxide might contribute to the vasodilatory effects of 17β-oestradiol in rat isolated coronary and mesenteric resistance arteries.