Effect of chronic treatment with 17beta-estradiol and progesterone on endothelium-dependent and endothelium-independent relaxation in isolated aortic rings from ovariectomized rats.

OBJECTIVE

Our purpose was to study the influence of chronic treatment with sex hormones on endothelium-dependent and endothelium-independent relaxation of rat aortic rings.

STUDY DESIGN

Rings of aortas, with and without endothelium, from rats treated with sex hormones or vehicle for 10 days were mounted in organ baths for isometric tension recording. Indomethacin (10(-5) mol/L) and N(omega)-nitro-L-arginine methyl ester (10(-4) mol/L), alone or in combination, were used to block cyclooxygenase and nitric oxide synthase, respectively. Mean data of contraction induced by potassium chloride (60 mmol/L), the relaxation by acetylcholine (10(-6) mol/L) in potassium chloride-contracted rings, tension induced by phenylephrine, and the negative logarithm of the concentration of acetylcholine or 3-morpholinosydnonimine producing a 50% relaxation, and area under the curve were calculated.

RESULTS

Treatment with 17beta-estradiol (10 microg/rat/day) decreased the tension induced by 60 mmol/L potassium chloride and increased the relaxation by acetylcholine in the rings with endothelium precontracted with potassium chloride. Contraction induced by potassium chloride and relaxation induced by acetylcholine were not influenced by the treatment with progesterone (2 mg/rat/day) or estrogen-progesterone combination. Treatment with estradiol, progesterone, or both hormones had no effect on tension developed in intact rings in response to phenylephrine and did not influence endothelium-dependent relaxation to acetylcholine or endothelium-independent relaxation to 3-morpholinosydnonimine in rings contracted with phenylephrine. The inhibition by N(omega)-nitro-L-arginine methyl ester of endothelium-dependent relaxation by acetylcholine was attenuated after the treatment with the sex hormones.

CONCLUSIONS

Chronic treatment with sex hormones did not increase production or release of endothelium-derived relaxing factor and did not change the sensitivity of rat aortic smooth muscle to nitric oxide. The treatment slightly counteracted the inhibition of endothelium-dependent relaxation produced by nitric oxide synthase blocker.