Epithelial Na+ channel (ENaC), hormones, and hypertension. - Wikidata - awgldk - TriplyDB

Epithelial Na+ channel (ENaC), hormones, and hypertension.

Epithelial Na+ channel (ENaC), hormones, and hypertension.

http://www.wikidata.org/entity/Q34025435

about

Genetics of resistant hypertension: a novel pharmacogenomics phenotype Sodium-retaining effect of insulin in diabetes Pharmacogenomics of hypertension and heart disease Impaired sodium excretion and salt-sensitive hypertension in corin-deficient mice Obesity-Associated Hypertension: the Upcoming Phenotype in African-American Women.The Concise Guide to PHARMACOLOGY 2013/14: ion channels Estrogen increases ENaC activity via PKCδ signaling in renal cortical collecting duct cells.Genetic variation in CYP4A11 and blood pressure response to mineralocorticoid receptor antagonism or ENaC inhibition: an exploratory pilot study in African Americans.Associations of epithelial sodium channel genes with blood pressure changes and hypertension incidence: the GenSalt study.Reduced expression of Enac in Placenta tissues of patients with severe preeclampsia is related to compromised trophoblastic cell migration and invasion during pregnancy.Urinary prostasin excretion is associated with adiposity in nonhypertensive African-American adolescents.mTORC2 regulates renal tubule sodium uptake by promoting ENaC activity.ENaC in the Rabbit Lacrimal Gland and its Changes During Sjögren Syndrome and Pregnancy.Chronic intrarenal insulin replacement reverses diabetes mellitus-induced natriuresis and diuresis.Inhibition of Mitochondrial Complex-1 Prevents the Downregulation of NKCC2 and ENaCα in Obstructive Kidney Disease.ENaCs and ASICs as therapeutic targets.A physiological concept unmasking vascular salt sensitivity in man Evaluation of the relationship between T663A polymorphism in the alpha-epithelial sodium channel gene and essential hypertension.Epoxyeicosatrienoic acids (EETs) regulate epithelial sodium channel activity by extracellular signal-regulated kinase 1/2 (ERK1/2)-mediated phosphorylation.Sub-chronic testosterone treatment increases the levels of epithelial sodium channel (ENaC)-α, β and γ in the kidney of orchidectomized adult male Sprague-Dawley rats.Sp1 trans-activates and is required for maximal aldosterone induction of the αENaC gene in collecting duct cells.Aldosterone reprograms promoter methylation to regulate αENaC transcription in the collecting duct.Sodium glucose transporter 2 (SGLT2) inhibition with empagliflozin improves cardiac diastolic function in a female rodent model of diabetes Deletion of α-subunit exon 11 of the epithelial Na+ channel reveals a regulatory module Physical and functional interaction of Rnf2 with Af9 regulates basal and aldosterone-stimulated transcription of the α-ENaC gene in a renal collecting duct cell line.Liddle syndrome in a Serbian family and literature review of underlying mutations.The importance of the ionic product for water to understand the physiology of the acid-base balance in humans.Vasopressin regulation of sodium transport in the distal nephron and collecting duct.Personalized Therapy of Hypertension: the Past and the Future.Controlling epithelial sodium channels with light using photoswitchable amilorides.Actions of Quercetin, a Polyphenol, on Blood Pressure.Prevalence of Liddle Syndrome Among Young Hypertension Patients of Undetermined Cause in a Chinese Population.Epithelial sodium channel inhibition by amiloride on blood pressure and cardiovascular disease risk in young prehypertensives.The influence of anti-hyperglycemic drug therapy on cardiovascular and heart failure outcomes in patients with type 2 diabetes mellitus.Novel mechanisms of Na+ retention in obesity: phosphorylation of NKCC2 and regulation of SPAK/OSR1 by AMPK.Liddle Syndrome: Review of the Literature and Description of a New Case.

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Epithelial Na+ channel (ENaC), hormones, and hypertension.

http://www.wikidata.org/entity/Q34025435

description

2010 nî lūn-bûn

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2010 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2010 թվականի մայիսին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Epithelial Na+ channel (ENaC), hormones, and hypertension.

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Epithelial Na+ channel (ENaC), hormones, and hypertension.

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Epithelial Na+ channel (ENaC), hormones, and hypertension.

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Epithelial Na+ channel (ENaC), hormones, and hypertension.

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Epithelial Na+ channel (ENaC), hormones, and hypertension.

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Epithelial Na+ channel (ENaC), hormones, and hypertension.

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Epithelial Na+ channel (ENaC), hormones, and hypertension.

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Epithelial Na+ channel (ENaC), hormones, and hypertension.

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Epithelial Na+ channel (ENaC), hormones, and hypertension.

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JBC.R109.025049

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Journal of Biological Chemistry

P1476

Epithelial Na+ channel (ENaC), hormones, and hypertension.

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James K Bubien

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P2860

Liddle's syndrome: heritable human hypertension caused by mutations in the beta subunit of the epithelial sodium channel

Regulation of Nedd4-2 self-ubiquitination and stability by a PY motif located within its HECT-domain

Nedd4-2 induces endocytosis and degradation of proteolytically cleaved epithelial Na+ channels

Salt-sensitive hypertension and cardiac hypertrophy in mice deficient in the ubiquitin ligase Nedd4-2

Serum aldosterone changes during hyperinsulinemia are correlated to body mass index and insulin sensitivity in patients with essential hypertension.

Narrative review: the emerging clinical implications of the role of aldosterone in the metabolic syndrome and resistant hypertension.

The endoplasmic reticulum-associated degradation of the epithelial sodium channel requires a unique complement of molecular chaperones.

Regulation of sodium transport by ENaC in the kidney

The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man.

Liddle's syndrome mutations increase Na+ transport through dual effects on epithelial Na+ channel surface expression and proteolytic cleavage.

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23527-23531

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scholarly article

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10.1074/JBC.R109.025049

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31

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285

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2010-05-11T00:00:00Z

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