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

Y. P. Vedernikov, Q. P. Liao, V. Jain, George Saade, K. Chwalisz, R. E. Garfield

Research output: Contribution to journalArticle

39 Citations (Scopus)

Abstract

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(ω)-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 17β-estradiol (10 μg/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(ω)-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.

Original languageEnglish (US)
Pages (from-to)603-608
Number of pages6
JournalAmerican Journal of Obstetrics and Gynecology
Volume176
Issue number3
DOIs
StatePublished - 1997

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Endothelium
Progesterone
Estradiol
Potassium Chloride
Acetylcholine
Gonadal Steroid Hormones
Phenylephrine
Therapeutics
Nitric Oxide Synthase
Endothelium-Dependent Relaxing Factors
Prostaglandin-Endoperoxide Synthases
Baths
Indomethacin
Area Under Curve
Smooth Muscle
Aorta
Nitric Oxide
Estrogens
Hormones

Keywords

  • endothelium-derived relaxing factor
  • nitric oxide
  • rat aorta
  • Sex hormones
  • vasodilatation

ASJC Scopus subject areas

  • Medicine(all)
  • Obstetrics and Gynecology

Cite this

Effect of chronic treatment with 17β-estradiol and progesterone on endothelium-dependent and endothelium-independent relaxation in isolated aortic rings from ovariectomized rats. / Vedernikov, Y. P.; Liao, Q. P.; Jain, V.; Saade, George; Chwalisz, K.; Garfield, R. E.

In: American Journal of Obstetrics and Gynecology, Vol. 176, No. 3, 1997, p. 603-608.

Research output: Contribution to journalArticle

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abstract = "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(ω)-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 17β-estradiol (10 μg/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(ω)-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.",
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T1 - Effect of chronic treatment with 17β-estradiol and progesterone on endothelium-dependent and endothelium-independent relaxation in isolated aortic rings from ovariectomized rats

AU - Vedernikov, Y. P.

AU - Liao, Q. P.

AU - Jain, V.

AU - Saade, George

AU - Chwalisz, K.

AU - Garfield, R. E.

PY - 1997

Y1 - 1997

N2 - 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(ω)-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 17β-estradiol (10 μg/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(ω)-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.

AB - 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(ω)-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 17β-estradiol (10 μg/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(ω)-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.

KW - endothelium-derived relaxing factor

KW - nitric oxide

KW - rat aorta

KW - Sex hormones

KW - vasodilatation

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