Estrogen and hypertension

Ashraf, Muhammad Shamvil; Vongpatanasin, Wanpen

doi:10.1007/s11906-006-0080-1

Cited by 140 publications

(98 citation statements)

References 97 publications

(109 reference statements)

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“…The E 2 -treated animals also required pressor support less frequently than controls, and the disparities in BP between the two groups remained apparent despite the differences in pressor support. Both endogenous and exogenous estrogens stimulate the hepatic synthesis of angiotensin that raises aldosterone via activation of the reninangiotensin system, and aldosterone causes renal sodium resorption, and these mechanisms may underlie the hypertension that can occur with oral contraceptive use (35,36). However, these processes are unlikely in the present study in which first- Figure 6.…”

Section: Discussionmentioning

confidence: 78%

“…Hart's staining indicated that elastic fibers were localized to both alveolar walls and septal tips (arrows) in lungs of (A) control-treated animals and primarily to emerging septal tips in (B) E 2 -treated lungs. In situ hybridization on serial sections similarly detected often intense elastin mRNA expression within alveolar walls and at emerging septae in (C) control group, and expression was localized primarily to emerging septae in ( pass hepatic metabolism of E 2 was avoided with cutaneous delivery of the hormone (36), and daily weights and urine output were not affected by E 2 treatment. Preterm human infants are at significant risk of hypotension and this is mimicked in the preterm baboon (37).…”

Section: Discussionmentioning

confidence: 82%

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Postnatal Estradiol Up-regulates Lung Nitric Oxide Synthases and Improves Lung Function in Bronchopulmonary Dysplasia

McCurnin

Pierce

Willis³

et al. 2009

Am J Respir Crit Care Med

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Rationale: Nitric oxide (NO) plays an important role in lung development and perinatal lung function, and pulmonary NO synthases (NOS) are decreased in bronchopulmonary dysplasia (BPD) following preterm birth. Fetal estradiol levels increase during late gestation and estradiol up-regulates NOS, suggesting that after preterm birth estradiol deprivation causes attenuated lung NOS resulting in impaired pulmonary function. Objective: To test the effects of postnatal estradiol administration in a primate model of BPD over 14 days after delivery at 125 days of gestation (term 5 185 d). Methods: Cardiopulmonary function was assessed by echocardiography and whole body plethysmography. Lung morphometric and histopathologic analyses were performed, and NOS enzymatic activity and abundance were measured. Measurements and Main Results: Estradiol caused an increase in blood pressure and ductus arteriosus closure. Expiratory resistance and lung compliance were also improved, and this occurred before spontaneous ductal closure. Furthermore, both oxygenation and ventilation indices were improved with estradiol, and the changes in lung function and ventilatory support requirements persisted throughout the study period. Whereas estradiol had negligible effect on indicators of lung inflammation and on lung structure assessed after the initial 14 days of ventilatory support, it caused an increase in lung neuronal and endothelial NOS enzymatic activity. Conclusions: In a primate model of BPD, postnatal estradiol treatment had favorable cardiovascular impact, enhanced pulmonary function, and lowered requirements for ventilatory support in association with an up-regulation of lung NOS. Estradiol may be an efficacious postnatal therapy to improve lung function and outcome in preterm infants.The signaling molecule nitric oxide (NO), generated by nitric oxide synthase (NOS), plays a key role in multiple processes in the mature lung (1, 2). In the developing lung, NO participates in pulmonary vascularization, alveolarization, and airway branching, and also counteracts apoptosis in multiple lung cell types (3-6). In the perinatal period, epithelium-derived NO is critically involved in the regulation of lung liquid production and of peripheral contractile elements (7, 8), and it also mediates pulmonary vasomotor tone (9). In studies of lungs from fetal baboons, we showed that all three NOS isoforms, neuronal NOS (nNOS), endothelial NOS (eNOS), and inducible NOS (iNOS), are principally expressed in proximal respiratory epithelium, and that there are maturational increases in their abundance and in NO production during the early third trimester (10). Thus, pulmonary NOS expression is up-regulated during fetal development in the primate, and this process may be critical to lung structural development and airway, parenchymal, and pulmonary vascular function in the early postnatal period.Bronchopulmonary dysplasia (BPD) is a devastating primary complication of premature birth that develops in the preterm human lung following ventilatory and oxyg...

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 82%

Postnatal Estradiol Up-regulates Lung Nitric Oxide Synthases and Improves Lung Function in Bronchopulmonary Dysplasia

McCurnin

Pierce

Willis³

et al. 2009

Am J Respir Crit Care Med

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“…28,29 In addition, estrogens inhibit the vasoconstrictor pathway mediated by the sympathetic nervous system and renin-angiotensin system. 30 We have shown that the CYP19A1 gene may be involved in the genetic regulation of BP in women and that this gene may have different roles depending on BMI. In a previous study, we reported that the effect of these two CYP19A1 variants in osteoporosis was also modified by BMI.…”

Section: Ramirez-lorca Et Al Cyp19a1 Variants and Regulation Of Bloodmentioning

confidence: 89%

Sex and Body Mass Index Specific Regulation of Blood Pressure by CYP19A1 Gene Variants

et al. 2007

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Abstract-Sexual dimorphism in blood pressure (BP) regulation has been observed both in humans and experimental animals, and estrogens have been shown to contribute to this epidemiological observation. A key enzyme in determining estrogen levels is aromatase cytochrome P450. The aim of this study was to evaluate the role of the gene encoding aromatase, CYP19A1, as an independent risk factor for hypertension and its relationship with systolic and diastolic BP measures. We genotyped 2 polymorphisms within the CYP19A1 gene, IVS4 rs11575899 and 3ЈUTR rs10046, in 3448 individuals. In quantitative analysis, we observed significant associations between the 2 polymorphisms and BP values in women, being these associations dependent on BMI and independent of menopause status. The case-control analysis revealed that the most prominent associations were found for nonobese women in diastolic hypertension (DHT) Key Words: essential hypertension Ⅲ body mass index Ⅲ polymorphism Ⅲ genetics Ⅲ estrogens Ⅲ gender E ssential hypertension (EH) is the most common cardiovascular disease, with a prevalence of nearly 27% worldwide. 1 EH is a major risk factor for stroke, heart disease, and end-stage renal disease. High arterial blood pressure is a complex and multifactorial disorder that results from the interaction of multiple genetic and environmental influences. 2 Genetic factors account for 30% to 50% of interindividual variability in blood pressure (BP), [3][4][5] and there is evidence suggesting that each of the polygenes contributing to hypertension has only a modest effect.Sexual dimorphism in the regulation of BP has been demonstrated in several population studies 3,6 and in experimental animal models. 7 Age-adjusted BP is consistently higher in men than women, but these differences are attenuated when women enter menopause. 8 These findings suggest the presence of distinct mechanisms of BP regulation in males and females, emphasizing the importance of the sex hormonal levels in determining BP. Thus, genes involved in testosterone-estradiol shunt are strong candidates to explain, at least in part, the genetic influence on hypertension. The aromatase cytochrome P450 is the enzyme responsible for catalyzing the final step of conversion of androgens into estrogens. 9 The importance of this enzyme in BP regulation has been highlighted in animal studies. Aromatase inhibitors have antihypertensive effects in rats with genetic and experimental hypertension. 10,11 Thus, genetic variations in CYP19A1, the gene encoding aromatase, might contribute to alterations in aromatase expression and enzyme activity,

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“…13 ER-dependent mechanisms regulating vascular tone include endothelium-independent vasodilation, increases in NO bioavailability, inhibition of vascular smooth muscle cell (VSMC) growth and excess proliferation after balloon injury, inhibition of the vascular renin-angiotensin-aldosterone system (RAAS) and the endothelin system, and inhibition of the sympathetic nervous system. 12,17,25,26 Preclinical studies have investigated the contribution of ER␣ and ER␤ for blood pressure, and the results suggest roles for both ER subtypes, depending on the animal model studied. 27 However, these data do not reflect human physiology or human ER function, nor do they take into account differences in ER function in healthy or diseased human arteries.…”

Section: Mechanisms Of Postmenopausal Hypertension Potential Role Of mentioning

confidence: 99%

“…69,70 In the context of hypertension in women, we would like to point out that hypertension is a frequent adverse effect in premenopausal women taking oral contraceptives. 26 In a prospective cohort study of 68 297 healthy premenopausal nurses, the relative risk of development of hypertension among users of oral contraceptives was 1.8 (95% CI: 1.5 to 2.3), even after adjustment for multiple other risk factors. 71 This risk decreases with time since cessation of oral contraceptives but still remains increased even after Ն6 years (relative risk: 1.2; 95% CI: 1.0 to 1.4).…”

Section: Animal Hormones ("Conjugated Equine Estrogens")mentioning

confidence: 99%

Postmenopausal Hypertension

2009

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H ypertension in women is often undiagnosed or inadequately treated, especially after menopause when cardiovascular risk increases. In premenopausal women, endogenous estrogens maintain vasodilation and thus contribute to blood pressure control. Aging and the loss of endogenous estrogen production after menopause are accompanied by increases in blood pressure, contributing to the high prevalence of hypertension in older women. Currently, Ϸ75% of postmenopausal women in the United States are hypertensive. The high prevalence of obesity, the lack of regular physical exercise, and dietary salt are important factors contributing to and aggravating postmenopausal hypertension. In view of the ongoing population aging throughout the world, diagnosis and treatment of hypertension in postmenopausal women are important to reduce the excess burden of associated cardiovascular disease and to improve outcomes of potentially fatal complications such as stroke and myocardial infarction. This article discusses current knowledge about the mechanisms and therapeutic issues related to postmenopausal hypertension. Hypertension: Important Determinant of Cardiovascular Risk in WomenMore than 25% of the female adult world population is hypertensive. 1 Elevations in blood pressure in women are related to cardiovascular risk (Figure, panel A), 2,3 with the prevalence of hypertension being particularly high among women aged Ն60 years. 1 In the United States, Ϸ75% of postmenopausal women are hypertensive. 4 Hypertension is often accompanied by other cardiovascular risk factors, eg, obesity, dyslipidemia, and diabetes mellitus. 5 It is noteworthy that the prevalence of hypertension-related cardiovascular complications is greater in postmenopausal women than in age-matched men. 6 Indeed, these complications represent the leading cause of death in women. 6 Clinical studies have documented beneficial effects of antihypertensive therapy on cardiovascular outcome, 5 even in patients Ն80 years of age. 7 Overall recognition, control, and treatment of hypertension in postmenopausal women are still poor in primary care, and hypertension is often not being treated aggressively enough. 4,8 -10 Thus, further improvements of medical and public health measures, awareness of patients and physicians, and improved information policies are needed. Blood Pressure and Endogenous Estrogens: Role of MenopausePrior to menopause, blood pressure is lower in women compared with age-matched men. 11,12 During the menstrual cycle, blood pressure levels are inversely related to circulating estrogen concentrations and lower when 17␤-estradiol levels peak, 12 reflecting the vasodilator activity of endogenous 17␤-estradiol. 13 Similarly, increases of endogenous estrogen production during pregnancy contribute to maintenance of normotension despite marked increases in plasma volume and cardiac output. 12,14 The first decade after menopause is accompanied by an increase in blood pressure ( Figure, panel B). 11,15 In the seventh decade of life, the prevalence of hypertension...

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Estrogen and hypertension

Cited by 140 publications

References 97 publications

Postnatal Estradiol Up-regulates Lung Nitric Oxide Synthases and Improves Lung Function in Bronchopulmonary Dysplasia

Postnatal Estradiol Up-regulates Lung Nitric Oxide Synthases and Improves Lung Function in Bronchopulmonary Dysplasia

Sex and Body Mass Index Specific Regulation of Blood Pressure by CYP19A1 Gene Variants

Postmenopausal Hypertension

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