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KMID : 0358320060470010055
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Korean Journal of Urology
2006 Volume.47 No. 1 p.55 ~ p.63
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The Effects of Estrogen on Neuronal Nitric Oxide Synthase Expression, Endothelial Nitric Oxide Synthase Expression and Vascular Endothelial Growth Factor Expression and on the Histologic Composition of Rat Uterus and Vagina
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Park Sung-Woo
Lee Jeong-Zoo
Lee Young-Jin
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Abstract
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Purpose: As suggested by many investigators, the cause of age-related female sexual dysfunction is the decline of serum estrogen. We investigated the effects of estrogen on the nitric oxide synthase(NOS) and vascular endothelial growth factor(VEGF) expressions and the histologic composition in the uterus and proximal and distal vagina of rats.
Materials and Methods: Forty-five mature female Sprague-Dawley rats were randomly divided into three groups; the control group(C), the oophorectomy group(O), and the estrogen replacement group(E). The expression rates of neuronal NOS(nNOS), endothelial NOS(eNOS), VEGF and the changes of the collagen component in the uterus and proximal and distal vaginal tissues were investigated by immunohistochemical staining and Masson’s trichrom staining.
Results: The expression rate of NOS was highest in the proximal vagina, and this was followed by the portion of the vagina distal to the uterus. The nNOS and eNOS expression rates were significantly decreased in the uterus and the proximal vagina of the E group(p＜0.05), and they were increased in the uterus and proximal vagina of the O group(p＜0.05). However, the VEGF expression rate was increased in only the uterus of E group. In all tissues, the collagen component was significantly decreased in the E group, while it was increased in the O group(p＜0.05).
Conclusions: These data suggest that estrogen downregulates nNOS and eNOS. In addition, estrogen deficiency induces collagen synthesis and it decreases the content of smooth muscle in the uterus and vagina, resulting in structural relaxation difficulty. (Korean J Urol 2006;47:55-63)
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KEYWORD
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Nitricoxide synthase, Vascular endothelial growth factor, Sexual dysfunctions, Estrogens
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