Estrogen maintains nitric oxide synthesis in arterioles of female hypertensive rats.
- 1 June 1997
- journal article
- research article
- Published by Ovid Technologies (Wolters Kluwer Health) in Hypertension
- Vol. 29 (6), 1351-1356
- https://doi.org/10.1161/01.hyp.29.6.1351
Abstract
Abstract We hypothesized that in female spontaneously hypertensive rats (SHR), estrogen moderates the dysfunction of arterioles by preserving nitric oxide synthesis. To this end, we conducted experiments on isolated gracilis muscle arterioles (approximately 55 μm in diameter) of 12-week-old SHR divided into four groups: females (fSHR), ovariectomized females (fSHR-OV), ovariectomized females with estrogen replacement (fSHR-OV+ES, 50 μg/kg SC 17β-estradiol benzoate every 48 hours), and males (mSHR). Arteriolar diameter in the presence of perfusion pressures of 60, 80, 100, and 120 mm Hg were obtained, and diameter changes were measured (at 80 mm Hg) in response to various concentrations of substance P (10 −9 to 5×10 −8 mol/L), sodium nitroprusside (10 −8 to 10 −6 mol/L), and A23187 (5×10 −8 to 10 −6 mol/L). The pressure-induced diameter of mSHR and fSHR-OV arterioles was significantly less (by approximately 10%) than that of fSHR and fSHR-OV+ES arterioles. N ω -nitro- l -arginine (10 −4 mol/L), a nitric oxide synthase inhibitor, elicited a significant decrease in basal arteriolar diameter of fSHR (by approximately 19%) and fSHR-OV+ES (by approximately 17%), thereby eliminating the differences in tone among the various groups. Dilations of fSHR and fSHR-OV+ES arterioles to substance P were significantly greater (by 140% at a concentration of 5×10 −8 mol/L) than those of mSHR and fSHR-OV arterioles, whereas dilations to sodium nitroprusside were not different among the groups. A23187 (a nitric oxide releaser) elicited dilations in arterioles of fSHR (5.9±1.5%, 13.0±1.8%, and 19.2±2.1%) and fSHR-OV+ES (4.3±1.0%, 10.3±2.4%, and 15.0±4.0%) but constrictions in those of mSHR (−7.5±1.6%, −25.3±39%, and −36.9±4.1%) and fSHR-OV (−2.6±1.7%, −7.4±3.3%, and −11.5±6.1%). We conclude that estrogen in fSHR is responsible for the preservation of nitric oxide synthesis in skeletal muscle arterioles, resulting in a greater modulation of pressure-induced myogenic tone than in mSHR and maintenance of nitric oxide–mediated dilations.Keywords
This publication has 18 references indexed in Scilit:
- Both nitric oxide and prostaglandin-mediated responses are impaired in skeletal muscle arterioles of hypertensive ratsJournal of Hypertension, 1996
- Gender Difference in Endothelial Dysfunction in the Aorta of Spontaneously Hypertensive RatsHypertension, 1995
- Circulating Nitric Oxide (Nitrite/Nitrate) Levels in Postmenopausal Women Substituted With 17β-Estradiol and Norethisterone AcetateHypertension, 1995
- Increased Expression of Endothelial Constitutive Nitric Oxide Synthase in Rat Aorta during PregnancyBiochemical and Biophysical Research Communications, 1994
- Circulating Nitrite/Nitrate Levels Increase with Follicular Development: Indirect Evidence for Estradiol-Mediated NO ReleaseBiochemical and Biophysical Research Communications, 1994
- Endothelial dysfunction augments myogenic arteriolar constriction in hypertension.Hypertension, 1993
- Relation between coronary risk and coronary mortality in women of the Renfrew and Paisley survey: comparison with menThe Lancet, 1992
- Reduced influence of nitric oxide on arteriolar tone in hypertensive Dahl rats.Hypertension, 1992
- Effects of Postmenopausal Estrogen Replacement on the Concentrations and Metabolism of Plasma LipoproteinsThe New England Journal of Medicine, 1991
- Estrogen-Binding Sites in Endothelial Cell CulturesScience, 1978