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Epithelial sodium channel

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https://www.readbyqxmd.com/read/29144530/liddle-s-syndrome-in-an-african-male-due-to-a-novel-frameshift-mutation-in-the-beta-subunit-of-the-epithelial-sodium-channel-gene
#1
Robert Freercks, Surita Meldau, Erika Jones, Jason Ensor, Clarise Weimers-Willard, Brian Rayner
Resistant hypertension is a common clinical problem in South Africa and is frequently associated with low renin and aldosterone levels, especially in black Africans. In South Africa, novel variants in the epithelial sodium channel (ENaC) have been described to be associated with varying degrees of hypokalaemia and hypertension due to primary sodium retention. We report here a case of Liddle's syndrome due to a novel c.1709del11 (p.Ser570Tyrfs*20) deletion in the beta-subunit of the ENaC in a young black African male...
September 23, 2017: Cardiovascular Journal of Africa
https://www.readbyqxmd.com/read/29137360/novel-mechanisms-for-crotonaldehyde-induced-lung-edema
#2
Yue Li, Jianjun Chang, Yong Cui, Runzhen Zhao, Yan Ding, Yapeng Hou, Zhiyu Zhou, Hong-Long Ji, Hongguang Nie
Background: Crotonaldehyde is a highly noxious α,β-unsaturated aldehyde in cigarette smoke that causes edematous acute lung injury. Objective: To understand how crotonaldehyde impairs lung function, we examined its effects on human epithelial sodium channels (ENaC), which are major contributors to alveolar fluid clearance. Methods: We studied alveolar fluid clearance in C57 mice and ENaC activity was examined in H441 cells. Expression of α- and γ-ENaC was measured at protein and mRNA levels by western blot and real-time PCR, respectively...
October 13, 2017: Oncotarget
https://www.readbyqxmd.com/read/29131643/electrophysiology-of-epithelial-sodium-channel-enac-embedded-in-supported-lipid-bilayer-using-a-single-nanopore-chip
#3
Muhammad Shuja Khan, Noura Sayed Dosoky, Ghulam Mustafa, Darayas Patel, Bakhrom K Berdiev, John Dalton Williams
Nanopore-based technologies are highly adaptable supports for developing label-free sensor chips to characterize lipid bilayers, membrane proteins and nucleotides. We utilized a single nanopore chip to study electrophysiology of epithelial Na+ channel (ENaC) incorporated in supported lipid membrane (SLM). An isolated nanopore was developed inside the silicon cavity followed by fusing large unilamellar vesicles (LUVs) of DPPS (1,2-dipalmitoyl-sn-glycero-3-phosphoserine) and DPPE (1,2-dipalmitoyl-sn-glycero-3-phosphoethanolamine) to produce a solvent-free SLM with giga-ohm (GΩ) sealed impedance...
November 13, 2017: Langmuir: the ACS Journal of Surfaces and Colloids
https://www.readbyqxmd.com/read/29129584/high-salt-loading-induces-urinary-storage-dysfunction-via-upregulation-of-epithelial-sodium-channel-alpha-in-the-bladder-epithelium-in-dahl-salt-sensitive-rats
#4
Seiji Yamamoto, Yuji Hotta, Kotomi Maeda, Tomoya Kataoka, Yasuhiro Maeda, Takashi Hamakawa, Yasuhiro Shibata, Shoichi Sasaki, Shinya Ugawa, Takahiro Yasui, Kazunori Kimura
We aimed to investigate whether high salt intake affects bladder function via epithelial sodium channel (ENaC) by using Dahl salt-resistant (DR) and salt-sensitive (DS) rats. Bladder weight of DR + high-salt diet (HS, 8% NaCl) and DS + HS groups were significantly higher than those of DR + normal-salt diet (NS, 0.3% NaCl) and DS + NS groups after one week treatment. We thereafter used only DR + HS and DS + HS group. Systolic and diastolic blood pressures were significantly higher in DS + HS group than in DR + HS group after the treatment period...
October 10, 2017: Journal of Pharmacological Sciences
https://www.readbyqxmd.com/read/29126194/central-and-peripheral-slow-pressor-mechanisms-contributing-to
#5
Jiao Lu, Hong-Wei Wang, Monir Ahmad, Marzieh Keshtkar-Jahromi, Mordecai P Blaustein, John Hamlyn, Frans H H Leenen
Aims: High salt intake markedly enhances hypertension induced by angiotensin II (Ang II). We explored central and peripheral slow-pressor mechanisms which may be activated by Ang II and salt. Methods and Results: In Protocol I, Wistar rats were infused subcutaneously with low- dose Ang II (150 ng/kg/min) and fed regular (0.4%) or high salt (2%) diet for 14 days. In Protocol II, Ang II -high salt was combined with intracerebroventricular infusion of mineralocorticoid receptor (MR) blockers (eplerenone, spironolactone), epithelial sodium channel (ENaC) blocker (benzamil), angiotensin II type 1 receptor (AT1R) blocker (losartan) or vehicles...
November 8, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/29123030/the-nonproton-ligand-of-acid-sensing-ion-channel-3-activates-mollusk-specific-fanac-channels-via-a-mechanism-independent-of-native-fmrfamide-peptide
#6
Xiao-Na Yang, You-Ya Niu, Yan Liu, Yang Yang, Wang Jin, Xiao-Yang Cheng, Hong Liang, Heng-Shan Wang, You-Min Hu, Xiang-Yang Lu, Michael X Zhu, Tian-Le Xu, Yun Tian, Ye Yu
The degenerin/epithelial sodium channel (DEG/ENaC) superfamily of ion channels contains subfamilies with diverse functions that are fundamental to many physiological and pathological processes, ranging from synaptic transmission to epileptogenesis. The absence in mammals of some DEG/ENaCs subfamily orthologs such as FMRFamide peptide-activated sodium channels (FaNaCs), which have been identified only in mollusks, indicates that the various subfamilies diverged early in evolution. We recently reported that the nonproton agonist 2-guanidine-4-methylquinazoline (GMQ) activates acid-sensing ion channels (ASICs), a DEG/ENaC subfamily mainly in mammals, in the absence of acidosis...
November 9, 2017: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/29107074/loss-of-%C3%AE-epithelial-sodium-channel-function-in-meibomian-glands-produces-pseudohypoaldosteronism-1-like-ocular-disease-in-mice
#7
Dongfang Yu, Yogesh Saini, Gang Chen, Andrew J Ghio, Hong Dang, Kimberlie A Burns, Yang Wang, Richard M Davis, Scott H Randell, Charles R Esther, Friedrich Paulsen, Richard C Boucher
Human subjects with pseudohypoaldosteronism-1 due to loss of function mutations in epithelial Na(+) channel (ENaC) subunits exhibit meibomian gland (MG) dysfunction. A conditional βENaC MG knockout mouse model was generated to elucidate the pathogenesis of absent ENaC function in the MG and associated ocular surface disease. βENaC MG KO mice exhibited a striking age dependent, female predominant MG dysfunction phenotype, with white toothpaste-like secretions observed obstructing MG orifices at seven weeks of age...
October 26, 2017: American Journal of Pathology
https://www.readbyqxmd.com/read/29102290/ion-channels-as-targets-to-treat-cystic-fibrosis-lung-disease
#8
S Lorraine Martin, Vinciane Saint-Criq, Tzyh-Chang Hwang, László Csanády
Lung health relies on effective mucociliary clearance and innate immune defence mechanisms. In cystic fibrosis (CF), an imbalance in ion transport due to an absence of chloride ion secretion, caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) and a concomitant sodium hyperabsorption, caused by dyregulation of the epithelial sodium channel (ENaC), results in mucus stasis which predisposes the lungs to cycles of chronic infection and inflammation leading to lung function decline...
October 25, 2017: Journal of Cystic Fibrosis: Official Journal of the European Cystic Fibrosis Society
https://www.readbyqxmd.com/read/29074490/lung-disease-phenotypes-caused-by-over-expression-of-combinations-of-alpha-beta-and-gamma-subunits-of-the-epithelial-sodium-channel-in-mouse-airways
#9
Alessandra Livraghi-Butrico, Kristen J Wilkinson, Allison S Volmer, Rodney C Gilmore, Troy D Rogers, Ray A Caldwell, Kimberlie A Burns, Charles R Esther, Marcus A Mall, Richard C Boucher, Wanda K O'Neal, Barbara R Grubb
The epithelial Na+ channel (ENaC) regulates airway surface hydration. In mouse airways, ENaC is composed of three subunits, alpha (α), beta (β), and gamma (γ), which are differentially expressed (α > β > γ). Airway-targeted overexpression of the β subunit results in Na+ hyperabsorption causing airway surface dehydration, hyperconcentrated mucus with delayed clearance, lung inflammation, and perinatal mortality. Notably, mice overexpressing the α or γ subunit do not exhibit airway Na+ hyperabsorption nor lung pathology...
October 26, 2017: American Journal of Physiology. Lung Cellular and Molecular Physiology
https://www.readbyqxmd.com/read/29069584/dendritic-cell-amiloride-sensitive-channels-mediate-sodium-induced-inflammation-and-hypertension
#10
Natalia R Barbaro, Jason D Foss, Dmytro O Kryshtal, Nikita Tsyba, Shivani Kumaresan, Liang Xiao, Raymond L Mernaugh, Hana A Itani, Roxana Loperena, Wei Chen, Sergey Dikalov, Jens M Titze, Bjorn C Knollmann, David G Harrison, Annet Kirabo
Sodium accumulates in the interstitium and promotes inflammation through poorly defined mechanisms. We describe a pathway by which sodium enters dendritic cells (DCs) through amiloride-sensitive channels including the alpha and gamma subunits of the epithelial sodium channel and the sodium hydrogen exchanger 1. This leads to calcium influx via the sodium calcium exchanger, activation of protein kinase C (PKC), phosphorylation of p47(phox), and association of p47(phox) with gp91(phox). The assembled NADPH oxidase produces superoxide with subsequent formation of immunogenic isolevuglandin (IsoLG)-protein adducts...
October 24, 2017: Cell Reports
https://www.readbyqxmd.com/read/29066445/collecting-duct-nitric-oxide-synthase-1%C3%A3-activation-maintains-sodium-homeostasis-during-high-sodium-intake-through-suppression-of-aldosterone-and-renal-angiotensin-ii-pathways
#11
Kelly A Hyndman, Elena V Mironova, Jorge F Giani, Courtney Dugas, Jessika Collins, Alicia A McDonough, James D Stockand, Jennifer S Pollock
BACKGROUND: During high sodium intake, the renin-angiotensin-aldosterone system is downregulated and nitric oxide signaling is upregulated in order to remain in sodium balance. Recently, we showed that collecting duct nitric oxide synthase 1β is critical for fluid-electrolyte balance and subsequently blood pressure regulation during high sodium feeding. The current study tested the hypothesis that high sodium activation of the collecting duct nitric oxide synthase 1β pathway is critical for maintaining sodium homeostasis and for the downregulation of the renin-angiotensin-aldosterone system-epithelial sodium channel axis...
October 24, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/29065098/effects-of-sodium-nitrite-on-renal-function-and-blood-pressure-in-hypertensive-vs-healthy-study-participants-a-randomized-placebo-controlled-crossover-study
#12
Jeppe B Rosenbæk, Bodil G Hornstrup, Andreas N Jørgensen, Jesper Mortensen, Erling B Pedersen, Jesper N Bech
OBJECTIVE: Nitric oxide is a key player in regulating vascular tone. Impaired endothelial nitric oxide synthesis plays an important role in hypertension. Replenishing of nitric oxide by sodium nitrite (NaNO2) has not been investigated in patients with essential hypertension (EHT). We aimed to determine the effects of NaNO2 on blood pressure (BP) and renal sodium and water regulation in patients with EHT compared with healthy control study participants (CON). METHODS: In a placebo-controlled, crossover study, we infused 240 μg NaNO2/kg/h or isotonic saline for 2 h in 14 EHT and 14 CON...
October 23, 2017: Journal of Hypertension
https://www.readbyqxmd.com/read/29061720/role-of-kidneys-in-sex-differences-in-angiotensin-ii-induced-hypertension
#13
Lei Wang, Ximing Wang, Helena Y Qu, Shan Jiang, Jie Zhang, Liying Fu, Jacentha Buggs, Bo Pang, Jin Wei, Ruisheng Liu
The significance of kidneys in regulation of sodium and water balance and hemodynamics has been demonstrated both in patients and animal models. In the present study, we tested our hypothesis that kidneys play an essential role in control of sex differences in angiotensin II (Ang II)-dependent hypertension. Kidney transplantations (KTXs) were performed between male (M) and female (F) C57BL/6 mice (donor→recipient: F→F, M→M, F→M, and M→F). Radiotelemetry transmitters were implanted for measurement of mean arterial pressure during the infusion of Ang II (600 ng·kg(-1)·min(-1))...
October 23, 2017: Hypertension
https://www.readbyqxmd.com/read/29055604/treatment-of-primary-graft-dysfunction-after-lung-transplantation-with-orally-inhaled-ap301-a-prospective-randomized-pilot-study
#14
Clemens Aigner, Alexis Slama, Maximilian Barta, Andreas Mitterbauer, Gyoergy Lang, Shahrokh Taghavi, Jose Matilla, Roman Ullrich, Katharina Krenn, Peter Jaksch, Klaus Markstaller, Walter Klepetko
BACKGROUND: Primary graft dysfunction (PGD) after lung transplantation (LTx) carries significant morbidity and mortality in the early post-operative period and is associated with the development of chronic lung allograft dysfunction. AP301, an activator of epithelial sodium channel-mediated Na(+) uptake represents a new concept for prevention and treatment of pulmonary edema and has shown promising results in the pre-clinical setting. This pilot study investigated the clinical effect of inhaled AP301 on patients with development of PGD > 1 according to International Society of Heart and Lung Transplantation criteria after primary LTx in a high-volume center and was conducted as a randomized, placebo-controlled, single-center pilot-study including 20 patients...
September 30, 2017: Journal of Heart and Lung Transplantation
https://www.readbyqxmd.com/read/29051045/angiotensin-ii-regulates-%C3%AE-enac-in-human-umbilical-vein-endothelial-cells
#15
Charles A Downs, Nicholle M Johnson, Camila Coca, My N Helms
The amiloride-sensitive epithelial sodium channel (ENaC) has been characterized in a variety of non-epithelial tissues. In the current study we sought to understand the effect of angiotensin II on δ ENaC function using human umbilical vein endothelial cells (HUVECs). The δ ENaC subunit is found in humans, but notably absent in rat and most mouse epithelial tissues. In this study we report the presence of δ ENaC in HUVECS with a half-life of ~80min and a change in δ ENaC abundance when HUVECs were treated with angiotensin II...
October 16, 2017: Microvascular Research
https://www.readbyqxmd.com/read/29045522/molecular-genetics-of-salt-sensitivity-and-hypertension-role-of-renal-epithelial-sodium-channel-genes
#16
Silvia R S Freitas
No abstract text is available yet for this article.
October 13, 2017: American Journal of Hypertension
https://www.readbyqxmd.com/read/29042083/aprotinin-prevents-proteolytic-epithelial-sodium-channel-enac-activation-and-volume-retention-in-nephrotic-syndrome
#17
Bernhard N Bohnert, Martina Menacher, Andrea Janessa, Matthias Wörn, Anja Schork, Sophie Daiminger, Hubert Kalbacher, Hans-Ulrich Häring, Christoph Daniel, Kerstin Amann, Florian Sure, Marko Bertog, Silke Haerteis, Christoph Korbmacher, Ferruh Artunc
Volume retention in nephrotic syndrome has been linked to activation of the epithelial sodium channel (ENaC) by proteolysis of its γ-subunit following urinary excretion of serine proteases such as plasmin. Here we tested whether pharmacological inhibition of urinary serine protease activity might protect from ENaC activation and volume retention in nephrotic syndrome. Urine from both nephrotic mice (induced by doxorubicin injection) and nephrotic patients exhibited high aprotinin-sensitive serine protease activity...
October 14, 2017: Kidney International
https://www.readbyqxmd.com/read/29040215/role-of-receptor-for-advanced-glycation-end-products-in-regulating-lung-fluid-balance-in-lipopolysaccharide-induced-acute-lung-injury-and-infection-related-acute-respiratory-distress-syndrome
#18
Hao Wang, Tao Wang, Zhicheng Yuan, Yufang Cao, Yongfang Zhou, Junyun He, Yongchun Shen, Ni Zeng, Luqi Dai, Fuqiang Wen, Lei Chen
Receptor for advanced glycation end products (RAGE) is implicated in inflammatory responses in acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), but its role in pulmonary edema formation remains unclear, especially in infection-related ARDS mainly caused by pneumonia or sepsis. In this study, we investigated the role of RAGE in alveolar fluid regulation by using RAGE gene knockout (RAGE) mice in a murine ALI model induced by lipopolysaccharide (LPS), and by comparing soluble RAGE (sRAGE) levels in serum and bronchial alveolar lavage fluid (BALF) between ARDS patients and control subjects...
October 16, 2017: Shock
https://www.readbyqxmd.com/read/29039242/computational-elucidation-mutational-and-hot-spot-based-designing-of-potential-inhibitors-against-human-acid-sensing-ion-channels-hasic-1a-to-treatment-of-various-physiological-conditions
#19
Anurag Singh Chauhan, Md Yousuf Ansari, Rani Mansuri, Manas Ranjan Dikhit, Vahab Ali, Ganesh Chandra Sahoo, Pradeep Das
Acid-sensing ion channels (ASICs) are ligand/proton-gated ion channels belonging to the family of the degenerin/epithelial Na(+) channel (DEG/ENaC). They function as a sodium-selective pore for Ca(2+) entry into neuronal cells during pathological conditions. The blocking of this channel has therapeutic importance, because at basal physiological pH (7.2), it is in a closed state and under a more acidic condition, and the ASIC1a ion channel is activated. To investigate the different states of the hASIC1a channel based on mutational analysis, structure based virtual screening and molecular dynamics simulation studies...
October 17, 2017: Journal of Biomolecular Structure & Dynamics
https://www.readbyqxmd.com/read/29036630/resequencing-epithelial-sodium-channel-genes-identifies-rare-variants-associated-with-blood-pressure-salt-sensitivity-the-gensalt-study
#20
Xiaoying Gu, Dongfeng Gu, Jiang He, Dabeeru C Rao, James E Hixson, Jichun Chen, Jianxin Li, Jianfeng Huang, Xigui Wu, Treva K Rice, Lawrence C Shimmin, Tanika N Kelly
BACKGROUND: A resequencing study of renal epithelial sodium channel (ENaC) genes was conducted to identify rare variants associated with BP salt-sensitivity. METHODS: The Genetic Epidemiology Network of Salt-Sensitivity (GenSalt) study was conducted among 1,906 participants who underwent a 7-day low-sodium followed by a 7-day high-sodium feeding-study. The 300 most salt-sensitive and 300 most salt-resistant GenSalt participants were selected for the resequencing study...
September 19, 2017: American Journal of Hypertension
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