Estrogen can modulate endothelial function in spontaneously hypertensive rats (SHR) by antioxidant mechanism (2001)
- Authors:
- USP affiliated authors: FORTES, ZULEICA BRUNO - ICB ; CARVALHO, MARIA HELENA CATELLI DE - ICB ; NIGRO, DOROTHY - ICB ; PASSAGLIA, RITA DE CASSIA ALEIXO TOSTES - ICB
- Unidade: ICB
- Assunto: FARMACOLOGIA
- Language: Inglês
- Abstract: In previous study we demonstrated that the decrease of ovarian hormones following ovariectomy aggravates the already exiting endothelial dysfunction in SHR [1]. The aim of this study was to evaluate whether estrogen attenuates endothelial dysfunction in SHR by an antioxidant mechanism. Vascular reactivity to acetylcholine (ACh), bradykinin (BK) (endothelium-dependent) and sodium nitroprusside (SNP) (endothelium-independent) was evaluated in mesenteric arteriolar bed isolated from SHR into physiological estrus (OE), ovariectomized (OVX), OVX treated with estradiol (E); estradiol+progesterone (E/P) or vitamin C (VitC). To evaluate whether the effects of estrogen depends on estrogen/receptor interaction OE and OVX were treated with estrogen receptor antagonist, tamoxifen (TX). Microvascular oxidative stress were evaluated by using intravital microscopy in mesentery microvessels in vivo superfused with hydroethidine, a reduced, nonfluorescent precursor of ethidium bromide. In the presence of oxidative challenge, hydroethidine is transformed intracellularly into ethidium bromide, which binds to DNA and is detected by virtue of its red fluorescence. A decreased relaxation to ACh (EC50; OVX: 2.9x10-8M vs OE: 1.1x10-8M; p<0.05) and Bk (Relaxation: OVX: 30.2±3.8 vs OE: 49.7±2.5; p<0.05) were observed in OVX. There were no differences on SNP responses. Hormonal and VitC treatments similarly restored endothelium-dependent vasodilatation in OVX. TX reducedendothelium-dependent relaxation in OE, but not in OVX The percentage of ethidium bromide-positive nuclei along the arteriolar wall in OVX (28.4±4.3; p<0.05) was significantly increased compared to OE (14.2±3.9). The OVX overproduction of oxyradicals was attenuated by E (15.7±2.2), E/P (14.8±0.8) and VitC (13.6±3.7). TX did not affect OE and OVX responses. Estrogen modulates endothelial function, in part, by a receptor-mediated system. However, the increased oxidative stress, which contributes to exacerbated endothelial dysfunction in OVX, is not dependent on estrogen/receptor interaction. [1] Hypertension.1999; 34: 914-919
- Imprenta:
- Publisher: Comissão de Cultura e Extensão Universitária do ICB/USP
- Publisher place: São Paulo
- Date published: 2001
- Source:
- Título: Resumos
- Conference titles: Congresso do Instituto de Ciências Biomédicas
-
ABNT
DANTAS, A P V et al. Estrogen can modulate endothelial function in spontaneously hypertensive rats (SHR) by antioxidant mechanism. 2001, Anais.. São Paulo: Comissão de Cultura e Extensão Universitária do ICB/USP, 2001. . Acesso em: 15 mar. 2026. -
APA
Dantas, A. P. V., Fortes, Z. B., Carvalho, M. H. C., Nigro, D., & Passaglia, R. de C. A. T. (2001). Estrogen can modulate endothelial function in spontaneously hypertensive rats (SHR) by antioxidant mechanism. In Resumos. São Paulo: Comissão de Cultura e Extensão Universitária do ICB/USP. -
NLM
Dantas APV, Fortes ZB, Carvalho MHC, Nigro D, Passaglia R de CAT. Estrogen can modulate endothelial function in spontaneously hypertensive rats (SHR) by antioxidant mechanism. Resumos. 2001 ;[citado 2026 mar. 15 ] -
Vancouver
Dantas APV, Fortes ZB, Carvalho MHC, Nigro D, Passaglia R de CAT. Estrogen can modulate endothelial function in spontaneously hypertensive rats (SHR) by antioxidant mechanism. Resumos. 2001 ;[citado 2026 mar. 15 ] - Intrauterine undernutrition in rats interferes with leukocyte migration, decreasing adhesion molecule expression in leukocytes and endothelial cells
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