Estrogen Induces Nitric Oxide Production Via Nitric Oxide Synthase Activation in Endothelial Cells

Nevzati, Edin; Shafighi, Maziar; Bakhtian, Kamran D.; Treiber, Hannes; Fandiño, Javier; Fathi, Ali-Reza

doi:10.1007/978-3-319-04981-6_24

Cited by 73 publications

(49 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Gonadal steroid hormones have direct actions on microglia, oligodendrocytes, neurons and endothelial cells that may contribute to alter the function of astrocytes (Chen and Lee, 2013;Habib et al, 2013;Pardes Habib et al, 2014b;Hirahara et al, 2013;J. Y. Lee et al, 2012;Lei et al, 2014;Nevzati et al, 2015; between species, brain regions and age. More recently a fourth type of glial cells has been described, known as NG2 cells or polydendrocytes (Levine et al, 1993;Stallcup et al, 1983;Wilson et al, 1981).…”

Section: Introductionmentioning

confidence: 96%

Regulation of astroglia by gonadal steroid hormones under physiological and pathological conditions

Acaz‐Fonseca

Ávila-Rodriguez

Garcia-Segura

et al. 2016

Progress in Neurobiology

104

View full text Add to dashboard Cite

Section: Introductionmentioning

confidence: 96%

Regulation of astroglia by gonadal steroid hormones under physiological and pathological conditions

Acaz‐Fonseca

Ávila-Rodriguez

Garcia-Segura

et al. 2016

Progress in Neurobiology

104

View full text Add to dashboard Cite

“…17β-estradiol activates BK channels directly [45]. BKβ1 is one of the downstream targets of sex hormones including 17β-estradiol and progesterone [46] and specifically activated by 17β-estradiol in the VSMCs [46]; increases neuronal nitric oxide synthase (nNOS) as well endothelial nitric oxide synthase (eNOS) expression; and releases NO in the endothelial cells, all of which promotes vasodilation [47,48]. …”

Section: Discussionmentioning

confidence: 99%

Menopause and Ischemic Stroke: A Brief Review

Shekhar

Travis

et al. 2017

MOJT

View full text Add to dashboard Cite

Ischemic stroke is one of the leading causes of morbidity and mortality worldwide. Females are protected against stroke before the onset of menopause. Menopause results in increased incidence of stroke when compared to men. The mechanisms of these differences remain to be elucidated. Considering that there is a postmenopausal phenomenon and females in general, are living longer sex hormone-dependent mechanisms have been postulated to be the primary factors responsible for the premenopausal protection from stroke and later to be responsible for the higher incidence and increased the severity of stroke after menopause. Animal studies suggest that administration of estrogen and progesterone is neuroprotective and decreases the incidence of stroke. However, the real-world outcomes of hormone replacement therapy have failed to decrease the stroke risk. Despite the multifactorial nature of sex differences in stroke, here, we briefly discuss the pathophysiology of sex steroid hormones, the molecular mechanisms of estrogen receptor-dependent signaling pathways in stroke, and the potential factors that determine the discrepant effects of hormone replacement therapy in stroke.

show abstract

“…The mechanisms controlling vasodilation through NO are complex and integrated with many biochemical pathways (Boeldt et al 2014). Elevated estrogen levels promote endothelium-dependent vasodilatation during normal pregnancy, which is mediated partly via NO through vascular smooth muscle relaxation (Nevzati et al 2015;Hayashi et al 1995). To understand the altered physiology of normal pregnancy via NO, an appreciation of NO metabolism is important.…”

Section: Physiology Of Arginine Homoarginine and Nitric Oxide In Prementioning

confidence: 99%

The role of arginine, homoarginine and nitric oxide in pregnancy

2015

View full text Add to dashboard Cite

Normal pregnancy leads to profound maternal hemodynamic changes, including increased blood volume and vasodilatation. Several vasodilator mediators are implicated, including prostaglandins, carbon monoxide and nitric oxide (NO). Pre-eclampsia (PE) affects 3-10 % of pregnancies and is associated with increased maternal and perinatal morbidity and mortality. Around 8 % of pregnancies are complicated by intra-uterine growth restriction (IUGR), also associated with increased perinatal mortality and morbidity. PE and IUGR often co-exist. NO is essential for the formation of healthy endothelium, and in pregnancy promotes endovascular invasion by the cytotrophoblast. As interstitial trophoblasts invade the maternal spiral arteries in the uterine wall, they produce NO which acts on artery walls to create a low-resistance, high-caliber uteroplacental unit. If this process fails, the result is a high-resistance uteroplacental circulation. The hypoperfused and ischemic placenta releases antiangiogenic factors which mediate generalized endothelial dysfunction, oxidative stress and inflammatory mediators. It is these mediators that are implicated in both the fetal and maternal syndromes of PE and IUGR. Studies of NO and its modulator amino acids, including the precursors arginine and homoarginine and the NO synthesis inhibitor asymmetric dimethylarginine (ADMA), have investigated their role in both normal and pathological pregnancies. Many studies of PE (and, to a lesser extent, IUGR) have investigated maternal circulating ADMA, arginine and homoarginine levels. This article reviews and discusses the role of these amino acids in pregnancy. The results have shed some light on their role in these pathologies, but some of the findings have been conflicting and more research is needed. Nevertheless, therapeutic interventions that manipulate these guanidine-amino acids and their interactions hold real promise for the management of pregnancies complicated by PE and/or IUGR, and the results of ongoing studies are eagerly awaited.

show abstract

Estrogen Induces Nitric Oxide Production Via Nitric Oxide Synthase Activation in Endothelial Cells

Cited by 73 publications

References 29 publications

Regulation of astroglia by gonadal steroid hormones under physiological and pathological conditions

Regulation of astroglia by gonadal steroid hormones under physiological and pathological conditions

Menopause and Ischemic Stroke: A Brief Review

The role of arginine, homoarginine and nitric oxide in pregnancy

Contact Info

Product

Resources

About