17β-Oestradiol enhances aortic endothelium function and smooth muscle contraction in male spontaneously hypertensive rats

17β-Oestradiol (E₂; oestrogen) is known to increase endothelium-dependent vasodilatation and NO (nitric oxide) production. It is also known to decrease the response of VSMCs (vascular smooth muscle cells) to vasoconstrictors in vitro. E₂ induces a decrease in age-related BP (blood pressure) development in MSHR (male spontaneously hypertensive rats). Whether this decrease is due to an effect on the endothelium or smooth muscle is unknown. To determine this effect, we examined the role of E₂ on vascular endothelium and smooth muscle separately. We treated MSHR with E₂ (2 mg·kg^-1 of body weight·week^-1) for 5–7 weeks and then examined the vasoconstrictor response in the intact and denuded rings (with or without endothelium respectively). SBP (systolic BP) was measured weekly. Aortic cGMP and cAMP contents, aortic vasoconstrictor response, endothelium suppression of the vasoconstrictor response and basal NO release from aortic rings were all measured at the end of the study. We found that the age-related development of SBP in MSHR was decreased in E₂-treated rats. The vascular response of denuded rings to a vasoconstrictor (phenylephrine and KCl) was increased in E₂-treated rats; however, this phenomenon was masked in intact rings. The enhanced endothelial function appears to override the E₂-increased smooth muscle vasoconstrictor response. Endothelium suppression, NO release and aortic cGMP content were all significantly higher in E₂-treated rats than in controls. Thus our results suggest that E₂ improves endothelium function; furthermore, the accompanied NO/cGMP increase and the endothelium suppression may be associated with an E₂-induced BP-lowering effect in MSHR.