Gender Differences in Vascular Reactivity to Endothelin-1 in Deoxycorticosterone-Salt Hypertensive Rats

Tostes, Rita C.; David, Flávia Lúcia; Carvalho, Maria Helena Catelli de; Nigro, Dorothy; Scivoletto, Regina; Fortes, Zuleica Bruno

doi:10.1097/00005344-200036001-00032

Cited by 21 publications

(31 citation statements)

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“…Our group showed that arteries from male, but not female, DOCA-salt rats display increased sensitivity to ET-1 and to the selective ET B receptor agonist IRL-1620 both in vitro and in vivo (47,48). Changes in ET Bmediated vascular responses were associated with increased ET-1 and ET B receptor gene expression in male, but not in female, animals (49).…”

Section: Endothelinmentioning

confidence: 96%

Effects of estrogen on the vascular system

Tostes

Nigro

Fortes

et al. 2003

Braz J Med Biol Res

174

126

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The cardiovascular protective actions of estrogen are partially mediated by a direct effect on the vessel wall. Estrogen is active both on vascular smooth muscle and endothelial cells where functionally competent estrogen receptors have been identified. Estrogen administration promotes vasodilation in humans and in experimental animals, in part by stimulating prostacyclin and nitric oxide synthesis, as well as by decreasing the production of vasoconstrictor agents such as cyclooxygenase-derived products, reactive oxygen species, angiotensin II, and endothelin-1. In vitro, estrogen exerts a direct inhibitory effect on smooth muscle by activating potassium efflux and by inhibiting calcium influx. In addition, estrogen inhibits vascular smooth muscle cell proliferation. In vivo, 17ß-estradiol prevents neointimal thickening after balloon injury and also ameliorates the lesions occurring in atherosclerotic conditions. As is the case for other steroids, the effect of estrogen on the vessel wall has a rapid non-genomic component involving membrane phenomena, such as alteration of membrane ionic permeability and activation of membrane-bound enzymes, as well as the classical genomic effect involving estrogen receptor activation and gene expression.

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Section: Endothelinmentioning

confidence: 96%

Effects of estrogen on the vascular system

Tostes

Nigro

Fortes

et al. 2003

Braz J Med Biol Res

174

126

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“…The inhibitory effects of estrogen on ET-1 levels are further supported by evidence from animal studies. Ovariectomized female animals show an increase in ET-1 levels in both plasma and vascular tissues, while supplementation with exogenous estrogen negates this increase in ET-1, suggesting a key role for estrogen on ET-1 expression (3,24,95,97,102).…”

Section: Sex Hormones and Endothelinmentioning

confidence: 99%

Endothelin in the female vasculature: a role in aging?

Lekontseva

Chakrabarti

Davidge

2010

American Journal of Physiology-Regulatory, Integrative and Comp

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vascular diseases are the leading cause of morbidity and mortality in the world. Aging is associated with an increased incidence of cardiovascular disease. Premenopausal women are relatively protected from vascular alterations compared with age-matched men, likely due to higher levels of the female sex hormones. However, these vasoprotective effects in women are attenuated after menopause. Thus, the vascular system in aging women is affected by both the aging process as well as loss of hormonal protection, positioning women of this age group at a high risk for cardiovascular diseases such as hypertension, myocardial infarction, and stroke. The endothelin system in general and endothelin-1 (ET-1) in particular plays an important role in the pathogenesis of vascular dysfunction associated with aging. Evidence suggests that the female sex steroids can interfere with the vascular expression and actions of ET-1 via several mechanisms, which may further contribute to pathological processes in the vasculature of aging women. In this review, we have summarized hormone-dependent vascular pathways whereby ET-1 may mediate the deleterious effects of aging in postmenopausal females.ET-1; menopause; estrogen; vasoconstriction; inflammation AGING OF THE VASCULAR SYSTEM is a complex process characterized by sustained proinflammatory and proconstrictor changes in the vascular microenvironment. The resulting structural and functional alterations in systemic vasculature lead to increased risk of cardiovascular diseases such as hypertension, myocardial infarction, and stroke in the aging population (12,18,51,70). In the absence of chronic preexisting conditions, such as diabetes, premenopausal women express a favorable cardiovascular phenotype compared with age-matched men, largely due to the vasoprotective role of ovarian steroids such as estrogen (92). An alteration in circulating sex hormones at menopause, such as the decrease in estrogens and a relative excess of androgens, is associated with the conversion from a low-to high-risk cardiovascular profile (19,56). Although the mechanisms underlying the pathogenesis of vascular dysfunction in postmenopausal women are not completely understood, it is believed to result from a complex interplay between the aging process and the decline in ovarian hormones like estrogen.Endothelin has emerged as one of the key mediators of vascular dysfunction and remodeling in aging. Interestingly, there is evidence that female sex steroids (in particular, estrogen) can regulate the endothelin system at various levels from gene transcription and posttranslational modification of the peptide to expression of its vascular receptors and postreceptor signaling events. This review will summarize current knowledge on the impact of aging and female sex hormones on the endothelin system, as well as outline directions where further research is needed. A better understanding of the role of endothelin in the pathogenesis of vascular dysfunction in postmenopausal women may lead to the development of novel sex-...

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“…For example, estrogen stimulates prostacyclin production in human vascular endothelial cells (31), and urinary excretion of prostacyclin increases in postmenopausal women receiving hormone therapy (32). In addition, the effect of estrogen may be related to the release of or sensitivity to endothelium-derived contracting factors such as endothelin-1 (33,34).…”

Section: Effects Of Estrogenmentioning

confidence: 99%

Decreases in Renal Functional Reserve and Proximal Tubular Fluid Output in Conscious Oophorectomized Rats

Nielsen¹,

Flyvbjerg²,

Bruun³

et al. 2003

Journal of the American Society of Nephrology

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Abstract. Age-dependent glomerulosclerosis with reduced GFR develops earlier among men than among women. Therefore, whether female sex hormones could prevent the agedependent decrease in GFR was investigated. The kidney function in oophorectomized rats treated with placebo (OOX group), estrogen (OOXϩE 2 group), or estrogen plus progesterone (OOXϩE 2 ϩP group) for 5 mo and in sham-operated rats (sham group) was examined. The rats were 13 mo of age at the time of the investigation. They were conscious and chronically instrumented. The results demonstrated that estrogen, alone or in combination with progesterone, was without effect on the baseline GFR and effective renal plasma flow but prevented severe decreases in the renal functional reserve and fractional proximal tubular fluid output (lithium clearance technique, fractional lithium excretion), which were observed in the OOX group. The renal functional reserve (estimated by stimulation with glycine) was Ϫ223 Ϯ 151, 483 Ϯ 129, 675 Ϯ 76, and 208 Ϯ 140 l/min in the OOX, OOXϩE 2 , OOXϩE 2 ϩP, and sham groups, respectively. Fractional lithium excretion was 12.4 Ϯ 3.1, 26.8 Ϯ 2.0, 31.8 Ϯ 2.5, and 23.6 Ϯ 3.3% in the OOX, OOXϩE 2 , OOXϩE 2 ϩP, and sham groups, respectively. In conclusion, oophorectomy at the age of 8 mo did not produce a decrease in baseline GFR in female rats within a period of 5 mo. However, oophorectomy led to severe decreases in the renal functional reserve and fractional proximal tubular fluid output. Both effects were prevented with administration of estrogen. Sham-operated rats demonstrated values for renal functional reserve and fractional lithium excretion that were between those observed for the OOX group and the groups treated with sex hormones.

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Gender Differences in Vascular Reactivity to Endothelin-1 in Deoxycorticosterone-Salt Hypertensive Rats

Cited by 21 publications

References 0 publications

Effects of estrogen on the vascular system

Effects of estrogen on the vascular system

Endothelin in the female vasculature: a role in aging?

Decreases in Renal Functional Reserve and Proximal Tubular Fluid Output in Conscious Oophorectomized Rats

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