Effects of transdermal estrogen replacement therapy on plasma levels of nitric oxide and plasma lipids in postmenopausal women

Balci, Hilal; Altunyurt, Sabahattin; Acar, Berrin; Fadiloğlu, Meral; Kırkalı, Güldal; Onvural, Banu

doi:10.1016/j.maturitas.2004.07.002

Cited by 14 publications

(9 citation statements)

References 26 publications

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“…Treated women in both groups showed a significant increase in endothelium-dependent vasodilation measured by ultrasonography of brachial artery and in the plasmatic nitrite/nitrate levels, which was not observed in placebo users. A significant increase in the NO metabolites levels has also been shown by Balci et al 80 with the use of transdermal 17β estradiol, 100 mg/week for 3 months.…”

Section: Hormone Therapy and Endothelial Functionsupporting

confidence: 59%

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Menopause, Estrogens, and Endothelial Dysfunction: Current Concepts

Maturana

Irigoyen

Spritzer

2007

Clinics

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Maturana MA, Irigoyen MC, Spritzer PM. Menopause, estrogens, and endothelial dysfunction: current concepts. Clinics. 2007;62(1):77-86. Menopause is defined as the permanent cessation of menses. Cardiovascular disease is the leading cause of death among postmenopausal women in developed countries. The disparity between the incidence of cardiovascular disease among women in pre-and postmenopause has been ascribed to the actions of endogenous estrogen on the cardiovascular system and, particularly, on the vascular endothelium. The endothelium plays an important role in cardiovascular homeostasis, either through the vascular tonus and its regulation, or through coagulation and the inflammatory response. Endothelial dysfunction is implicated in the genesis of atherosclerosis and other chronic disorders, such as diabetes mellitus and hypertension. The pharmacological use of estrogen exerts influence on the circulating levels of markers of vascular tonus, and inflammation, as well as prothrombotic, and fibrinolytic markers, but the impact of these changes on the atherosclerotic disease is still uncertain.

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Section: Hormone Therapy and Endothelial Functionsupporting

confidence: 59%

“…22 Again, the results are influenced by environmental and physiological factors. Greater reproducibility and smaller intrapatient variability of the test are related to preconstriction of the tested vessel, ideally about 80% of the vein constriction in the basal state (ED 80 ). 39 …”

Section: Impedance Plethysmography and Dorsal Hand Vein Compliancementioning

confidence: 99%

Menopause, Estrogens, and Endothelial Dysfunction: Current Concepts

Maturana

Irigoyen

Spritzer

2007

Clinics

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“…Clinical studies suggest that estrogen reduces LDL-cholesterol levels and increases HDL-cholesterol levels in post-menopausal women [80], [81]. Furthermore, estrogen deficiency may decrease rates of triglyceride metabolism by down-regulating transcription factors such as PPARA [82], a key regulator of lipid metabolism.…”

Section: Discussionmentioning

confidence: 99%

Transcriptional Profiling of Human Liver Identifies Sex-Biased Genes Associated with Polygenic Dyslipidemia and Coronary Artery Disease

et al. 2011

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Sex-differences in human liver gene expression were characterized on a genome-wide scale using a large liver sample collection, allowing for detection of small expression differences with high statistical power. 1,249 sex-biased genes were identified, 70% showing higher expression in females. Chromosomal bias was apparent, with female-biased genes enriched on chrX and male-biased genes enriched on chrY and chr19, where 11 male-biased zinc-finger KRAB-repressor domain genes are distributed in six clusters. Top biological functions and diseases significantly enriched in sex-biased genes include transcription, chromatin organization and modification, sexual reproduction, lipid metabolism and cardiovascular disease. Notably, sex-biased genes are enriched at loci associated with polygenic dyslipidemia and coronary artery disease in genome-wide association studies. Moreover, of the 8 sex-biased genes at these loci, 4 have been directly linked to monogenic disorders of lipid metabolism and show an expression profile in females (elevated expression of ABCA1, APOA5 and LDLR; reduced expression of LIPC) that is consistent with the lower female risk of coronary artery disease. Female-biased expression was also observed for CYP7A1, which is activated by drugs used to treat hypercholesterolemia. Several sex-biased drug-metabolizing enzyme genes were identified, including members of the CYP, UGT, GPX and ALDH families. Half of 879 mouse orthologs, including many genes of lipid metabolism and homeostasis, show growth hormone-regulated sex-biased expression in mouse liver, suggesting growth hormone might play a similar regulatory role in human liver. Finally, the evolutionary rate of protein coding regions for human-mouse orthologs, revealed by dN/dS ratio, is significantly higher for genes showing the same sex-bias in both species than for non-sex-biased genes. These findings establish that human hepatic sex differences are widespread and affect diverse cell metabolic processes, and may help explain sex differences in lipid profiles associated with sex differential risk of coronary artery disease.

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“…Both endothelial nitric oxide synthase and neuronal nitric oxide synthase are tightly regulated by estrogen (85). The higher NO bioavailability offered by estrogen is likely responsible for the beneficial cardiovascular effect of the female gender (86,87). One of the key downstream signaling molecules of NO is the serine/threonine protein kinase Akt with a key role in cardiac survival and function (88).…”

Section: Neurovascular Regulation Of Metabolic Syndrome In Heartsmentioning

confidence: 99%

Cardiac Health in Women With Metabolic Syndrome: Clinical Aspects and Pathophysiology

Ren

Kelley

2009

Obesity

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Although the classical cardiovascular risk factors (e.g., smoking and hypertension) are becoming more effectively managed, a continuous increase of the so-called "cardiometabolic risk" is noted. Starting from this century, the nomenclature "metabolic syndrome" has become more popular to identify a cluster of disorders including obesity, dyslipidemia, hypertension, and insulin resistance. It is a primary risk factor for diabetes and cardiovascular disease in both genders. Interestingly, the metabolic diseases display a distinct gender disparity with an apparent "female advantage" in the premenopausal women compared with age-matched men. However, women usually lose such "sex protection" following menopause or affliction of metabolic syndrome especially insulin resistance. A controversy exists in the medical literature concerning whether metabolic syndrome is a real syndrome or simply a cluster of risk factors. Several scenarios are speculated to contribute to the gender dimorphism in the cardiovascular sequelae in patients with metabolic syndrome including sex hormones, intrinsic organ function, and the risk factor profile (e.g., hypertension, dyslipidemia, obesity, sedentary lifestyle, and atherogenic diet). With the alarming rise of obesity prevalence, heart problems in metabolic syndrome continue to rise with a distinct gender dimorphism. Although female hearts seem to better tolerate the stress insults compared with the male counterparts, the female sex hormones such as estrogen can interact with certain risk factors to precipitate myopathic changes in the hearts. This synthetic review of recent literature suggests a role of gender disparity in myopathic factors and risk attributable to each metabolic component in the different prevalence of metabolic syndrome.

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Effects of transdermal estrogen replacement therapy on plasma levels of nitric oxide and plasma lipids in postmenopausal women

Cited by 14 publications

References 26 publications

Menopause, Estrogens, and Endothelial Dysfunction: Current Concepts

Menopause, Estrogens, and Endothelial Dysfunction: Current Concepts

Transcriptional Profiling of Human Liver Identifies Sex-Biased Genes Associated with Polygenic Dyslipidemia and Coronary Artery Disease

Cardiac Health in Women With Metabolic Syndrome: Clinical Aspects and Pathophysiology

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