2003
DOI: 10.1016/s1071-55760300049-2
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Estrogen Selectively Up-Regulates eNOS and nNOS in Reproductive Arteries By Transcriptional Mechanisms

Abstract: Basal eNOS and nNOS isoform expression is greatest in arteries from reproductive tissues, and isoform responses to E(2)beta are cell specific and transcriptionally regulated. Furthermore, optimal uterine vascular responses to acute E(2)beta exposure require daily E(2)beta exposure that enhances basal NOS expression and abundance.

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Cited by 38 publications
(62 citation statements)
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“…The importance of the NOS3-NO system during pregnancy has recently been reinforced by the findings that uterine artery remodeling is impaired and litter size is reduced in NOS3-null compared to wild-type mice (van der Heijden et al, 2005). In vivo, there is solid evidence showing that uterine artery endothelial NOS3 protein is increased during pregnancy Magness et al, 2001) and in the follicular phase of the estrous cycle or by estrogen replacement therapy in association with elevated circulating estrogen levels (Chen et al, 2006;Rosenfeld et al, 2003;Rupnow et al, 2001;. Available data also suggest that uterine artery endothelial NOS3 expression can be regulated at the level of transcription (Rosenfeld et al, 2003).…”
Section: Disscussionmentioning
confidence: 99%
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“…The importance of the NOS3-NO system during pregnancy has recently been reinforced by the findings that uterine artery remodeling is impaired and litter size is reduced in NOS3-null compared to wild-type mice (van der Heijden et al, 2005). In vivo, there is solid evidence showing that uterine artery endothelial NOS3 protein is increased during pregnancy Magness et al, 2001) and in the follicular phase of the estrous cycle or by estrogen replacement therapy in association with elevated circulating estrogen levels (Chen et al, 2006;Rosenfeld et al, 2003;Rupnow et al, 2001;. Available data also suggest that uterine artery endothelial NOS3 expression can be regulated at the level of transcription (Rosenfeld et al, 2003).…”
Section: Disscussionmentioning
confidence: 99%
“…In vivo, there is solid evidence showing that uterine artery endothelial NOS3 protein is increased during pregnancy Magness et al, 2001) and in the follicular phase of the estrous cycle or by estrogen replacement therapy in association with elevated circulating estrogen levels (Chen et al, 2006;Rosenfeld et al, 2003;Rupnow et al, 2001;. Available data also suggest that uterine artery endothelial NOS3 expression can be regulated at the level of transcription (Rosenfeld et al, 2003). Despite significant efforts have been paid to the regulation of NOS3 expression in the uterine and placental circulations, the mechanism(s) controlling uterine and placental artery endothelial NOS3 expression currently remains unknown.…”
Section: Disscussionmentioning
confidence: 99%
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“…An enhanced response to KCl in arteries of the betamethasone group was also evident after known vasodilatory pathways were blocked. Nitric oxide and prostanoids affecting vasomotor activity are considered to originate predominantly from endothelium, however, in some vascular beds smooth muscle production of these bioactive molecules is known to occur (20,21). The larger response to KCl in L-NAME pretreated arteries suggests that, in sheep brachial artery, there may be contribution of the smooth muscle to NO production.…”
Section: Discussionmentioning
confidence: 99%