FIGURE 8.

Attenuation by oestradiol of ML213‐mediated relaxation is not endothelium dependent. Mean data for ML213‐mediated relaxation of pre‐constricted arterial tone (U46619; 300 nmol·L⁻¹) in arteries from female Wistar rats in di‐oestrus/met‐oestrus (F‐D/M; a, b; n = 6–8) or pro‐oestrus/oestrus (F‐P/E; c, d; n = 5–6) in the presence and absence of endothelial cells (ECs(+)/(−)) and in the absence of endothelial cells pre‐incubated in oestradiol (E2, 10 nmol·L⁻¹; EC(−) + E2). Mean data and scatter plot for carbachol (CCh)‐mediated relaxation of pre‐contracted arterial tone (10 μmol·L⁻¹ methoxamine) generated within the same vessels prior to application of ML213 (b, d). Relative fold expression in oestrogen receptors (Esr1, Esr2 and Gper1), EC marker Cd31 and vascular smooth muscle marker Acta2 in whole lysates of mesenteric arteries from female Wistar rats in vessels denuded of endothelium (EC(−)) compared with vessels with intact endothelium (EC(+); 2^−ΔΔCq; n = 5; e). Data shown are means ± SEM; n = number of animals used. * P ≤ 0.05, significantly different from EC(+); $ P ≤ 0.05, significant difference between EC(+) and EC(−) + 10 nM E2; # P ≤ 0.05, significant difference between EC(−) and EC(−) + 10 nM E2: two‐way ANOVA with post hoc Bonferroni test.