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- W2801693799 abstract "Postmenopausal period has been associated to different symptoms such as hot flashes, vulvovaginal atrophy, hypoactive sexual desire disorder (HSDD) and others. Clinical studies have described postmenopausal women presenting HSDD can benefit from the association of testosterone to conventional hormonal therapy. Testosterone has been linked to development of cardiovascular diseases including hypertension and it also increases cytochrome P-450-induced 20-HETE synthesis which in turn results in vascular dysfunction. However, the effect of testosterone plus estrogen in the cardiovascular system is still very poorly studied. The aim of the present study is to evaluate the role of cytochrome P-450 pathway in a postmenopausal hypertensive female treated with testosterone plus estrogen. For that, hypertensive ovariectomized rats (OVX-SHR) were used as a model of postmenopausal hypertension and four groups were created: SHAM-operated (SHAM), ovariectomized SHR (OVX), OVX treated for 15 days with conjugated equine estrogens [(CEE) 9.6 μg/Kg/day/po] or CEE associated to testosterone [(CEE+T) 2.85 mg/kg/weekly/im]. Phenylephrine-induced contraction and generation of reactive oxygen species (ROS) were markedly increased in aortic rings from OVX-SHR compared to SHAM rats which were restored by CEE treatment. On the other hand, CEE+T abolished vascular effects by CEE and augmented both systolic and diastolic blood pressure of SHR. Treatment of aortic rings with the CYP/20-HETE synthesis inhibitor HET0016 (1 μM) reduced phenylephrine hyperreactivity and the augmented ROS generation in the CEE+T group. These results are paralleled by the increased CYP4F3 protein expression and activity in aortas of CEE+T. In conclusion, we showed that association of testosterone to estrogen therapy produces detrimental effects in cardiovascular system of ovariectomized hypertensive females via CYP4F3/20-HETE pathway. Therefore, our findings support the standpoint that the CYP/20-HETE pathway is an important therapeutic target for the prevention of cardiovascular disease in menopausal women in the presence of high levels of testosterone." @default.
- W2801693799 created "2018-05-17" @default.
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- W2801693799 date "2018-05-08" @default.
- W2801693799 modified "2023-10-17" @default.
- W2801693799 title "Detrimental Effects of Testosterone Addition to Estrogen Therapy Involve Cytochrome P-450-Induced 20-HETE Synthesis in Aorta of Ovariectomized Spontaneously Hypertensive Rat (SHR), a Model of Postmenopausal Hypertension" @default.
- W2801693799 cites W1571327998 @default.
- W2801693799 cites W184377109 @default.
- W2801693799 cites W1913730804 @default.
- W2801693799 cites W1941875192 @default.
- W2801693799 cites W1965541556 @default.
- W2801693799 cites W1966207709 @default.
- W2801693799 cites W1968265290 @default.
- W2801693799 cites W1981256690 @default.
- W2801693799 cites W1981699771 @default.
- W2801693799 cites W1982046698 @default.
- W2801693799 cites W1987718059 @default.
- W2801693799 cites W1988734218 @default.
- W2801693799 cites W1991765235 @default.
- W2801693799 cites W1995142464 @default.
- W2801693799 cites W1998513025 @default.
- W2801693799 cites W2004405160 @default.
- W2801693799 cites W2007439146 @default.
- W2801693799 cites W2009579364 @default.
- W2801693799 cites W2016706063 @default.
- W2801693799 cites W2018368054 @default.
- W2801693799 cites W2019411611 @default.
- W2801693799 cites W2020529112 @default.
- W2801693799 cites W2022342720 @default.
- W2801693799 cites W2024142910 @default.
- W2801693799 cites W2034628038 @default.
- W2801693799 cites W2035988407 @default.
- W2801693799 cites W2037647348 @default.
- W2801693799 cites W2039527118 @default.
- W2801693799 cites W2039679069 @default.
- W2801693799 cites W2040909870 @default.
- W2801693799 cites W2041781505 @default.
- W2801693799 cites W2043421724 @default.
- W2801693799 cites W2052771434 @default.
- W2801693799 cites W2059266278 @default.
- W2801693799 cites W2066134098 @default.
- W2801693799 cites W2068726505 @default.
- W2801693799 cites W2069568986 @default.
- W2801693799 cites W2077997462 @default.
- W2801693799 cites W2079546402 @default.
- W2801693799 cites W2095017261 @default.
- W2801693799 cites W2097523109 @default.
- W2801693799 cites W2097683472 @default.
- W2801693799 cites W2100800289 @default.
- W2801693799 cites W2103856091 @default.
- W2801693799 cites W2104868466 @default.
- W2801693799 cites W2105250244 @default.
- W2801693799 cites W2105864994 @default.
- W2801693799 cites W2107782429 @default.
- W2801693799 cites W2109535176 @default.
- W2801693799 cites W2113257066 @default.
- W2801693799 cites W2115263295 @default.
- W2801693799 cites W2118665083 @default.
- W2801693799 cites W2119165558 @default.
- W2801693799 cites W2119860475 @default.
- W2801693799 cites W2121079663 @default.
- W2801693799 cites W2125007558 @default.
- W2801693799 cites W2133047862 @default.
- W2801693799 cites W2136619969 @default.
- W2801693799 cites W2138431834 @default.
- W2801693799 cites W2140424613 @default.
- W2801693799 cites W2143027656 @default.
- W2801693799 cites W2147111955 @default.
- W2801693799 cites W2147971048 @default.
- W2801693799 cites W2148525491 @default.
- W2801693799 cites W2150644859 @default.
- W2801693799 cites W2160423145 @default.
- W2801693799 cites W2160939922 @default.
- W2801693799 cites W2162639891 @default.
- W2801693799 cites W2167117857 @default.
- W2801693799 cites W2168349092 @default.
- W2801693799 cites W2168769524 @default.
- W2801693799 cites W2168801830 @default.
- W2801693799 cites W2168980353 @default.
- W2801693799 cites W2169595519 @default.
- W2801693799 cites W2171926119 @default.
- W2801693799 cites W2177913759 @default.
- W2801693799 cites W2199314512 @default.
- W2801693799 cites W2218822201 @default.
- W2801693799 cites W2319299237 @default.
- W2801693799 cites W2336300998 @default.
- W2801693799 cites W2398951544 @default.
- W2801693799 cites W2411836675 @default.
- W2801693799 cites W2411838644 @default.
- W2801693799 cites W2413356861 @default.