Endothelin, Kidney Disease, and Hypertension

Speed, Joshua S.; Pollock, David M.

doi:10.1161/hypertensionaha.113.00595

Cited by 50 publications

(48 citation statements)

References 47 publications

(64 reference statements)

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“…However, endothelin-1 activates renal afferent nerves during high salt intake in normal kidneys, 58 and is implicated in progression of CKD. 5 Therefore, endothelin-1 may be implicated but this was not investigated in this study. The mechanism whereby efferent renal nerve activity upregulates the renal epithelial RAS was not established.…”

Section: Discussionmentioning

confidence: 89%

“…1,2 Fibrosis is estimated to contribute to 45% of all causes of mortality 3 and is promoted by many factors present in damaged kidneys and CKD, including oxidative stress, inflammation, hypertension, hypoxia, metabolic toxins, and activation of the sympathetic nervous system (SNS). [4][5][6][7][8][9][10][11][12] The association of hypertensive renal disease with dietary salt is well recognized. [13][14][15][16] Many patients with CKD have salt-sensitive hypertension.…”

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confidence: 99%

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A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression

Cao

Wang

et al. 2015

Journal of the American Society of Nephrology

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Salt intake promotes progression of CKD by uncertain mechanisms. We hypothesized that a salt-induced reno-cerebral reflex activates a renin-angiotensin axis to promote CKD. Sham-operated and 5/6-nephrectomized rats received a normal-salt (0.4%), low-salt (0.02%), or high-salt (4%) diet for 2 weeks. High salt in 5/6-nephrectomized rats increased renal NADPH oxidase, inflammation, BP, and albuminuria. Furthermore, high salt activated the intrarenal and cerebral, but not the systemic, renin-angiotensin axes and increased the activity of renal sympathetic nerves and neurons in the forebrain of these rats. Renal fibrosis was increased 2.2-fold by high versus low salt, but intracerebroventricular tempol, losartan, or clonidine reduced this fibrosis by 65%, 69%, or 59%, respectively, and renal denervation or deafferentation reduced this fibrosis by 43% or 38%, respectively (all P,0.05). Salt-induced fibrosis persisted after normalization of BP with hydralazine. These data suggest that the renal and cerebral renin-angiotensin axes are interlinked by a reno-cerebral reflex that is activated by salt and promotes oxidative stress, fibrosis, and progression of CKD independent of BP.

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Section: Discussionmentioning

confidence: 89%

mentioning

confidence: 99%

A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression

Cao

Wang

et al. 2015

Journal of the American Society of Nephrology

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“…Endothelin-1 (ET-1) is a 21-amino-acid, mainly endothelium-derived, peptide with vasoconstrictive, inflammatory and mitogenic properties [8][9][10][11]. Elevated ET-1 levels have been associated with hypertension, endothelial dysfunction and atherosclerotic diseases [9,[12][13][14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

Plasma levels of endothelin-1 and renal function among young and healthy adults

Fischer

Bossard

Aeschbacher

et al. 2017

Clinical Chemistry and Laboratory Medicine (CCLM)

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Background: Endothelin-1 (ET-1), a vasoconstrictive and pro-inflammatory peptide, is associated with several cardiovascular risk factors and outcomes. We aimed to investigate the association of plasma ET-1 levels and renal function among young and healthy adults. Methods: Individuals aged 25-41 years were enrolled in a population-based cohort study. Main exclusion criteria were established kidney disease, cardiovascular diseases, diabetes mellitus and a body mass index > 35 kg/m 2 .

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“…39 The kidneys are extremely sensitive to ET-1 and the components of ET system are present throughout the nephron and renal vasculature. 40 ET-1 is produced by glomerular epithelial and mesangial 41 Accordingly, ET-1 is thought of particular importance in the progression of chronic kidney disease. The ET system is chronically activated in dia- betic patients with DN as evidenced by elevated circulating levels of ET-1 9 , increased kidney ET-1 concentrations 42 , and increased renal and systemic ETA receptor activation 43 .…”

Section: Discussionmentioning

confidence: 99%

Endothelin-1 Gene Polymorphisms rs5370, rs1476046, and rs3087459 are not Associated with Diabetic Nephropathy in Caucasians with Type 2 Diabetes Mellitus

et al. 2017

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Materials and methods:The study population consisted of 651 Caucasian subjects with T2DM of more than 10 years' duration: 276 patients with DN (cases) and 375 patients without evidence of DN (controls). Polymorphisms in ET-1 (EDN1) gene, rs5370, rs1476046, and rs3087459, were studied. Results: Genotype distributions of the studied polymorphisms showed no significant diff erence between cases and controls. Conclusions: We provide evidence that the rs5370, rs1476046, and rs3087459 polymorphisms of EDN1 gene are not risk factors for DN in Caucasians with T2DM.

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Endothelin, Kidney Disease, and Hypertension

Cited by 50 publications

References 47 publications

A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression

A Salt-Induced Reno-Cerebral Reflex Activates Renin-Angiotensin Systems and Promotes CKD Progression

Plasma levels of endothelin-1 and renal function among young and healthy adults

Endothelin-1 Gene Polymorphisms rs5370, rs1476046, and rs3087459 are not Associated with Diabetic Nephropathy in Caucasians with Type 2 Diabetes Mellitus

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