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Hormonal modulation of endothelial NO production

Since the discovery of endothelium-derived relaxing factor and the subsequent identification of nitric oxide (NO) as the primary mediator of endothelium-dependent relaxations, research has focused on chemical and physical stimuli that modulate NO levels. Hormones represent a class of soluble, widely... Full description

Journal Title: Pflügers Archiv 2010-03-07, Vol.459 (6), p.841-851
Main Author: Duckles, Sue P
Other Authors: Miller, Virginia M
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Berlin/Heidelberg: Springer-Verlag
ID: ISSN: 0031-6768
Link: https://www.ncbi.nlm.nih.gov/pubmed/20213497
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2865573
title: Hormonal modulation of endothelial NO production
format: Article
creator:
  • Duckles, Sue P
  • Miller, Virginia M
subjects:
  • Androgens - physiology
  • Animals
  • Article
  • Biomedical and Life Sciences
  • Biomedicine
  • Cell Biology
  • Corticosteroids
  • Endothelium
  • Endothelium, Vascular - physiology
  • Endothelium-derived relaxing factors
  • Enzymes
  • Estrogen
  • Estrogens - physiology
  • Female
  • Glucocorticoids
  • Glucocorticoids - physiology
  • Growth factor
  • Growth Hormone - physiology
  • Growth hormones
  • Hormones - physiology
  • Human Physiology
  • Humans
  • Insulin
  • Insulin - physiology
  • Invited Review
  • Male
  • Metabolic disorders
  • Molecular Medicine
  • Neurosciences
  • Nitric oxide
  • Nitric Oxide - biosynthesis
  • Nitric Oxide Synthase Type III
  • Physiological aspects
  • Progesterone
  • Progesterone - physiology
  • Prolactin
  • Receptor, IGF Type 1 - physiology
  • Receptor, Insulin - physiology
  • Receptors
  • Receptors, Estrogen - physiology
  • Receptors, Glucocorticoid - physiology
  • Receptors, Progesterone - physiology
  • Receptors, Somatotropin - physiology
  • Somatotropin
  • Testosterone
ispartof: Pflügers Archiv, 2010-03-07, Vol.459 (6), p.841-851
description: Since the discovery of endothelium-derived relaxing factor and the subsequent identification of nitric oxide (NO) as the primary mediator of endothelium-dependent relaxations, research has focused on chemical and physical stimuli that modulate NO levels. Hormones represent a class of soluble, widely circulating chemical factors that impact production of NO both by rapid effects on the activity of endothelial nitric oxide synthase (eNOS) through phosphorylation of the enzyme and longer term modulation through changes in amount of eNOS protein. Hormones that increase NO production including estrogen, progesterone, insulin, and growth hormone do so through both of these common mechanisms. In contrast, some hormones, including glucocorticoids, progesterone, and prolactin, decrease NO bioavailability. Mechanisms involved include binding to repressor response elements on the eNOS gene, competing for co-regulators common to hormones with positive genomic actions, regulating eNOS co-factors, decreasing substrate for eNOS, and increasing production of oxygen-derived free radicals. Feedback regulation by the hormones themselves as well as the ability of NO to regulate hormonal release provides a second level of complexity that can also contribute to changes in NO levels. These effects on eNOS and changes in NO production may contribute to variability in risk factors, presentation of and treatment for cardiovascular disease associated with aging, pregnancy, stress, and metabolic disorders in men and women.
language: eng
source:
identifier: ISSN: 0031-6768
fulltext: no_fulltext
issn:
  • 0031-6768
  • 1432-2013
url: Link


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descriptionSince the discovery of endothelium-derived relaxing factor and the subsequent identification of nitric oxide (NO) as the primary mediator of endothelium-dependent relaxations, research has focused on chemical and physical stimuli that modulate NO levels. Hormones represent a class of soluble, widely circulating chemical factors that impact production of NO both by rapid effects on the activity of endothelial nitric oxide synthase (eNOS) through phosphorylation of the enzyme and longer term modulation through changes in amount of eNOS protein. Hormones that increase NO production including estrogen, progesterone, insulin, and growth hormone do so through both of these common mechanisms. In contrast, some hormones, including glucocorticoids, progesterone, and prolactin, decrease NO bioavailability. Mechanisms involved include binding to repressor response elements on the eNOS gene, competing for co-regulators common to hormones with positive genomic actions, regulating eNOS co-factors, decreasing substrate for eNOS, and increasing production of oxygen-derived free radicals. Feedback regulation by the hormones themselves as well as the ability of NO to regulate hormonal release provides a second level of complexity that can also contribute to changes in NO levels. These effects on eNOS and changes in NO production may contribute to variability in risk factors, presentation of and treatment for cardiovascular disease associated with aging, pregnancy, stress, and metabolic disorders in men and women.
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languageeng
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subjectAndrogens - physiology ; Animals ; Article ; Biomedical and Life Sciences ; Biomedicine ; Cell Biology ; Corticosteroids ; Endothelium ; Endothelium, Vascular - physiology ; Endothelium-derived relaxing factors ; Enzymes ; Estrogen ; Estrogens - physiology ; Female ; Glucocorticoids ; Glucocorticoids - physiology ; Growth factor ; Growth Hormone - physiology ; Growth hormones ; Hormones - physiology ; Human Physiology ; Humans ; Insulin ; Insulin - physiology ; Invited Review ; Male ; Metabolic disorders ; Molecular Medicine ; Neurosciences ; Nitric oxide ; Nitric Oxide - biosynthesis ; Nitric Oxide Synthase Type III ; Physiological aspects ; Progesterone ; Progesterone - physiology ; Prolactin ; Receptor, IGF Type 1 - physiology ; Receptor, Insulin - physiology ; Receptors ; Receptors, Estrogen - physiology ; Receptors, Glucocorticoid - physiology ; Receptors, Progesterone - physiology ; Receptors, Somatotropin - physiology ; Somatotropin ; Testosterone
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descriptionSince the discovery of endothelium-derived relaxing factor and the subsequent identification of nitric oxide (NO) as the primary mediator of endothelium-dependent relaxations, research has focused on chemical and physical stimuli that modulate NO levels. Hormones represent a class of soluble, widely circulating chemical factors that impact production of NO both by rapid effects on the activity of endothelial nitric oxide synthase (eNOS) through phosphorylation of the enzyme and longer term modulation through changes in amount of eNOS protein. Hormones that increase NO production including estrogen, progesterone, insulin, and growth hormone do so through both of these common mechanisms. In contrast, some hormones, including glucocorticoids, progesterone, and prolactin, decrease NO bioavailability. Mechanisms involved include binding to repressor response elements on the eNOS gene, competing for co-regulators common to hormones with positive genomic actions, regulating eNOS co-factors, decreasing substrate for eNOS, and increasing production of oxygen-derived free radicals. Feedback regulation by the hormones themselves as well as the ability of NO to regulate hormonal release provides a second level of complexity that can also contribute to changes in NO levels. These effects on eNOS and changes in NO production may contribute to variability in risk factors, presentation of and treatment for cardiovascular disease associated with aging, pregnancy, stress, and metabolic disorders in men and women.
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5Cell Biology
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14Glucocorticoids
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41Receptors, Progesterone - physiology
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abstractSince the discovery of endothelium-derived relaxing factor and the subsequent identification of nitric oxide (NO) as the primary mediator of endothelium-dependent relaxations, research has focused on chemical and physical stimuli that modulate NO levels. Hormones represent a class of soluble, widely circulating chemical factors that impact production of NO both by rapid effects on the activity of endothelial nitric oxide synthase (eNOS) through phosphorylation of the enzyme and longer term modulation through changes in amount of eNOS protein. Hormones that increase NO production including estrogen, progesterone, insulin, and growth hormone do so through both of these common mechanisms. In contrast, some hormones, including glucocorticoids, progesterone, and prolactin, decrease NO bioavailability. Mechanisms involved include binding to repressor response elements on the eNOS gene, competing for co-regulators common to hormones with positive genomic actions, regulating eNOS co-factors, decreasing substrate for eNOS, and increasing production of oxygen-derived free radicals. Feedback regulation by the hormones themselves as well as the ability of NO to regulate hormonal release provides a second level of complexity that can also contribute to changes in NO levels. These effects on eNOS and changes in NO production may contribute to variability in risk factors, presentation of and treatment for cardiovascular disease associated with aging, pregnancy, stress, and metabolic disorders in men and women.
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