Mechanisms of vasorelaxation to 17β-oestradiol in rat arteries

• Published in: European journal of pharmacology 2003-08, Vol.476 (1), p.139-149
• Main Authors: Tep-areenan, Patcharin, Kendall, David A., Randall, Michael D.
• Format: Article
• Language: English
• Subjects: 17β-Oestradiol; Biological and medical sciences; Ca 2+ influx; Hormones. Endocrine system; K + channel; Medical sciences; Pharmacology. Drug treatments; Vasorelaxation
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/S0014-2999(03)02152-6

We have investigated the involvement of the endothelium, K + channels, oestradiol receptors, and Ca 2+ influx in 17β-oestradiol-induced vasorelaxation in rat mesenteric arterial beds and aortae. 17β-Oestradiol (10 pM–1 mM) caused acute vasorelaxations in mesenteric arterial beds and aortae from male and female rats. In male rat mesenteric vessels and aortae, the vasorelaxations were mostly independent of the endothelium and nitric oxide (NO). However, indomethacin (10 μM) enhanced the relaxant responses to 17β-oestradiol. In male rat mesenteric beds, 60 mM KCl, tetrabutylammonium chloride (300 μM), 4-aminopyridine (1 mM), and barium chloride (30 μM), charybdotoxin (100 nM), but not glibenclamide (10 μM) and tamoxifen (10 μM), inhibited vasorelaxation to 17β-oestradiol. In male rat aortae, 60 mM KCl did not affect vasorelaxation to 17β-oestradiol. However, in the presence of indomethacin, vasorelaxation to 17β-oestradiol was enhanced but this was sensitive to 60 mM KCl. Pre-treatment with 17β-oestradiol (100 μM) inhibited CaCl 2-induced contraction. The present findings indicate that, in rat mesenteric beds and aortae, 17β-oestradiol causes acute and potent vasorelaxation which may be enhanced in the presence of a cyclooxygenase inhibitor. In mesenteric arterial bed, 17β-oestradiol-induced vasorelaxation occurs primarily via activation of K + channels. In the aorta, vasorelaxations involved activation of K + efflux when the cyclooxygenase pathway was inhibited, and also inhibition of Ca 2+ influx.