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Epithelial sodium channel

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https://www.readbyqxmd.com/read/28528375/hypothalamic-signaling-in-body-fluid-homeostasis-and-hypertension
#1
REVIEW
Brian J Kinsman, Haley N Nation, Sean D Stocker
PURPOSE OF REVIEW: The central nervous system plays a pivotal role in the regulation of extracellular fluid volume and consequently arterial blood pressure. Key hypothalamic regions sense and integrate neurohumoral signals to subsequently alter intake (thirst and salt appetite) and output (renal excretion via neuroendocrine and autonomic function). Here, we review recent findings that provide new insight into such mechanisms that may represent new therapeutic targets. RECENT FINDINGS: Implementation of cutting edge neuroscience approaches such as opto- and chemogenetics highlight pivotal roles of circumventricular organs to impact body fluid homeostasis...
June 2017: Current Hypertension Reports
https://www.readbyqxmd.com/read/28484659/systemic-pseudohypoaldosteronism-type-i-a-case-report-and-review-of-the-literature
#2
Nasifa Nur, Cameron Lang, Juanita K Hodax, Jose Bernardo Quintos
Systemic pseudohypoaldosteronism (PHA) type I is a rare genetic disorder resulting from mutations in the subunits of the epithelial sodium channel that manifests as severe salt wasting, hyperkalemia, and metabolic acidosis in infancy. In this article we report a patient with systemic PHA type I presenting with severe dehydration due to salt wasting at 6 days of life. She was found to have a known mutation in the SCNN1A gene and subsequently required treatment with sodium supplementation. We also review the clinical presentation, differential diagnosis, and treatment of systemic PHA type I and summarize data from 27 cases with follow-up data...
2017: Case Reports in Pediatrics
https://www.readbyqxmd.com/read/28481660/spx-101-is-a-novel-enac-targeted-therapeutic-for-cystic-fibrosis-that-restores-mucus-transport
#3
David W Scott, Matthew P Walker, Juliana Sesma, Bryant Wu, Timothy J Stuhlmiller, Juan R Sabater, William M Abraham, Timothy M Crowder, Dale J Christensen, Robert Tarran
RATIONALE: Cystic Fibrosis lung disease (CF) is caused by the loss of function of the cystic fibrosis transmembrane conductance regulator (CFTR) combined with hyperactivation of the epithelial sodium channel (ENaC). In the lung, ENaC is responsible for movement of sodium which creates an osmotic gradient that pulls fluid out of the airway. Hyperactivation of ENaC contributes to reduced airway hydration causing mucus dehydration, decreased mucociliary clearance, and chronic bacterial infections...
May 8, 2017: American Journal of Respiratory and Critical Care Medicine
https://www.readbyqxmd.com/read/28480509/oxidized-low-density-lipoprotein-stimulates-epithelial-sodium-channels-in-endothelial-cells-of-mouse-thoracic-aorta
#4
Chen Liang, Qiu-Shi Wang, Xu Yang, Na Niu, Qing-Qing Hu, Bao-Long Zhang, Ming-Ming Wu, Chang-Jiang Yu, Xiao Chen, Bin-Lin Song, Zhi-Ren Zhang, He-Ping Ma
BACKGROUND AND PURPOSE: Epithelial sodium channel (ENaC) is expressed in endothelial cells and acts as a negative modulator of vasodilation. Oxidized low-density lipoprotein (ox-LDL) is a key pathological factor in endothelial dysfunction. The present study is to examine the role of ENaC in ox-LDL-induced endothelial dysfunction and its associated signal transduction pathway. EXPERIMENTAL APPROACH: Patch-clamp techniques combined with pharmacological approaches were used to examine ENaC activity in the endothelial cells of split-open mouse thoracic aorta...
May 8, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28473772/lack-of-effects-of-metformin-and-aicar-chronic-infusion-on-the-development-of-hypertension-in-dahl-salt-sensitive-rats
#5
Tengis S Pavlov, Vladislav Levchenko, Daria V Ilatovskaya, Hui Li, Oleg Palygin, Nuria M Pastor-Soler, Kenneth R Hallows, Alexander Staruschenko
In the kidney, reabsorption via the epithelial sodium channel (ENaC) is involved in long-term blood pressure control. Previously we demonstrated that ENaC hyperactivity is associated with development of salt-sensitive (SS) hypertension in Dahl SS rats. AMP-activated kinase (AMPK), playing a role in cellular energy homeostasis, has been shown to decrease ENaC activity. Here, we tested whether metformin and AICAR, two drugs that activate AMPK, affect the development of salt-induced hypertension. High salt diet significantly increased mean arterial pressure (MAP) in Dahl SS rats...
2017: Frontiers in Physiology
https://www.readbyqxmd.com/read/28468944/enac-activity-is-regulated-by-calpain-2-proteolysis-of-marcks-proteins
#6
Darrice S Montgomery, Ling Yu, Zinah M Ghazi, Tiffany L Thai, Otor Al-Khalili, He-Ping Ma, Douglas C Eaton, Abdel A Alli
We previously demonstrated a role for the myristoylated alanine-rich C kinase substrate (MARCKS) to serve as an adaptor protein in the anionic phospholipid phosphate-dependent regulation of the epithelial sodium channel (ENaC). Both MARCKS and ENaC are regulated by proteolysis. Calpains are a family of ubiquitously expressed intracellular Ca(2+)-dependent cysteine proteases involved in signal transduction. Here we examine the role of calpain-2 in regulating MARCKS and ENaC in cultured renal epithelial cells and in the mouse kidney...
May 3, 2017: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/28458673/inflammatory-responses-regulating-alveolar-ion-transport-during-pulmonary-infections
#7
REVIEW
Christin Peteranderl, Jacob I Sznajder, Susanne Herold, Emilia Lecuona
The respiratory epithelium is lined by a tightly balanced fluid layer that allows normal O2 and CO2 exchange and maintains surface tension and host defense. To maintain alveolar fluid homeostasis, both the integrity of the alveolar-capillary barrier and the expression of epithelial ion channels and pumps are necessary to establish a vectorial ion gradient. However, during pulmonary infection, auto- and/or paracrine-acting mediators induce pathophysiological changes of the alveolar-capillary barrier, altered expression of epithelial Na,K-ATPase and of epithelial ion channels including epithelial sodium channel and cystic fibrosis membrane conductance regulator, leading to the accumulation of edema and impaired alveolar fluid clearance...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28446807/increased-blood-pressure-in-nesfatin-nuclebindin-2-transgenic-mice
#8
Yusaku Mori, Hiroyuki Shimizu, Hideki Kushima, Munenori Hiromura, Michishige Terasaki, Michitaka Tanaka, Aya Osaki, Tsutomu Hirano
Nesfatin/nucleobindin-2 (nesf/NUCB2), a precursor of the anorexigenic protein nesfatin-1, is selectively expressed in the hypothalamic nuclei, which are central to the regulation of the autonomic nervous system. The present study sought to investigate the involvement of nesf/NUCB2 in the regulation of blood pressure and ingestive behavior, by using nesf/NUCB2-transgenic (Tg) mice. Blood pressure and heart rates were measured under conscious and unconscious conditions. Twenty-four-hour water intake and urine volume of male nesf/NUCB2-Tg mice and their littermates in metabolic cages were measured...
April 27, 2017: Hypertension Research: Official Journal of the Japanese Society of Hypertension
https://www.readbyqxmd.com/read/28442491/constitutively-active-spak-causes-hyperkalemia-by-activating-ncc-and-remodeling-distal-tubules
#9
P Richard Grimm, Richard Coleman, Eric Delpire, Paul A Welling
Aberrant activation of with no lysine (WNK) kinases causes familial hyperkalemic hypertension (FHHt). Thiazide diuretics treat the disease, fostering the view that hyperactivation of the thiazide-sensitive sodium-chloride cotransporter (NCC) in the distal convoluted tubule (DCT) is solely responsible. However, aberrant signaling in the aldosterone-sensitive distal nephron (ASDN) and inhibition of the potassium-excretory renal outer medullary potassium (ROMK) channel have also been implicated. To test these ideas, we introduced kinase-activating mutations after Lox-P sites in the mouse Stk39 gene, which encodes the terminal kinase in the WNK signaling pathway, Ste20-related proline-alanine-rich kinase (SPAK)...
April 25, 2017: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/28439270/cytokine-regulation-of-na-k-cl-cotransporter-1-and-cystic-fibrosis-transmembrane-conductance-regulator-potential-role-in-pulmonary-inflammation-and-edema-formation
#10
REVIEW
Sarah Weidenfeld, Wolfgang M Kuebler
Pulmonary edema, a major complication of lung injury and inflammation, is defined as accumulation of extravascular fluid in the lungs leading to impaired diffusion of respiratory gases. Lung fluid balance across the alveolar epithelial barrier protects the distal airspace from excess fluid accumulation and is mainly regulated by active sodium transport and Cl(-) absorption. Increased hydrostatic pressure as seen in cardiogenic edema or increased vascular permeability as present in inflammatory lung diseases such as the acute respiratory distress syndrome (ARDS) causes a reversal of transepithelial fluid transport resulting in the formation of pulmonary edema...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28424211/connecting-tubule-glomerular-feedback-mediates-tubuloglomerular-feedback-resetting-post-unilateral-nephrectomy
#11
Sumit R Monu, Yilin Ren, J X Masjoan Juncos, Kristopher Kutskill, Hong Wang, Nitin Kumar, Edward L Peterson, Oscar A Carretero
Unilaterally nephrectomized rats (UNx) have higher glomerular capillary pressure (PGC) that can cause significant glomerular injury in the remnant kidney. PGC is controlled by the ratio of afferent (Af-Art) and efferent arteriole resistance. Af-Art resistance in turn is regulated by two intrinsic feedback mechanisms: 1) Tubuloglomerular feedback (TGF) that causes Af-Art constriction in response to increased NaCl in the macula densa and 2) connecting tubule glomerular feedback (CTGF) that causes Af-Art dilatation in response to an increase in NaCl transport in the connecting tubule via the epithelial sodium channel (ENaC)...
April 19, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28409833/dietary-salt-blunts-vasodilation-by-stimulating-epithelial-sodium-channels-in-endothelial-cells-from-salt-sensitive-rats
#12
Zi-Rui Wang, Hui-Bin Liu, Ying-Ying Sun, Qing-Qing Hu, Yu-Xia Li, Wei-Wan Zheng, Chang-Jiang Yu, Xin-Yuan Li, Ming-Ming Wu, Bin-Lin Song, Jian-Jun Mu, Zu-Yi Yuan, Zhi-Ren Zhang, He-Ping Ma
BACKGROUND AND PURPOSE: Our recent studies show that the reduced activity of epithelial sodium channels (ENaC) in endothelial cells accounts for the adaptation of vasculature to salt in Sprague-Dawley (SD) rats. The present study examines a hypothesis that enhanced ENaC activity mediates the loss of vasorelaxation in Dahl salt-sensitive (SS) rats. EXPERIMENTAL APPROACH: We used the cell-attached patch-clamp technique to record ENaC activity in split-open mesenteric arteries...
April 13, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28405801/urine-exosomes-from-healthy-and-hypertensive-pregnancies-display-elevated-level-of-%C3%AE-subunit-and-cleaved-%C3%AE-and-%C3%AE-subunits-of-the-epithelial-sodium-channel-enac
#13
Maria R Nielsen, Britta Frederiksen-Møller, Rikke Zachar, Jan S Jørgensen, Mie R Hansen, Rikke Ydegaard, Per Svenningsen, Kristian Buhl, Boye L Jensen
Preeclampsia is characterized by hypertension, proteinuria, suppression of plasma renin-angiotensin-aldosterone, and impaired urine sodium excretion. Aberrantly filtered plasmin in urine may activate proteolytically the γ-subunit of the epithelial sodium channel (ENaC) and promote Na(+) reabsorption and urine K(+) loss. Plasma and urine was sampled from patients with preeclampsia, healthy pregnant controls and non-pregnant women, and from patients with nephrostomy catheters. Aldosterone concentration, urine plasminogen, and protein were determined...
April 12, 2017: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/28396810/management-of-liddle-syndrome-in-pregnancy-a-case-report-and-literature-review
#14
Michael Awadalla, Manasi Patwardhan, Adham Alsamsam, Nashat Imran
Liddle syndrome is an autosomal dominant genetic condition that causes hypertension and hypokalemia due to a gain-of-function mutation in the SCNN1B or SCNN1G genes which code for the epithelial sodium channel in the kidney. This leads to increased sodium and water reabsorption causing hypertension. We report a case of a 27-year-old pregnant woman who was admitted for hypertension and hypokalemia and later diagnosed and treated for Liddle syndrome using amiloride. Maintaining a high suspicion of Liddle syndrome in pregnancy is essential in such cases to be able to adequately and effectively treat the hypertension...
2017: Case Reports in Obstetrics and Gynecology
https://www.readbyqxmd.com/read/28386087/delivery-of-enac-sirna-to-epithelial-cells-mediated-by-a-targeted-nanocomplex-a-therapeutic-strategy-for-cystic-fibrosis
#15
Maria D I Manunta, Aristides D Tagalakis, Martin Attwood, Ahmad M Aldossary, Josephine L Barnes, Mustafa M Munye, Alexander Weng, Robin J McAnulty, Stephen L Hart
The inhibition of ENaC may have therapeutic potential in CF airways by reducing sodium hyperabsorption, restoring lung epithelial surface fluid levels, airway hydration and mucociliary function. The challenge has been to deliver siRNA to the lung with sufficient efficacy for a sustained therapeutic effect. We have developed a self-assembling nanocomplex formulation for siRNA delivery to the airways that consists of a liposome (DOTMA/DOPE; L), an epithelial targeting peptide (P) and siRNA (R). LPR formulations were assessed for their ability to silence expression of the transcript of the gene encoding the α-subunit of the sodium channel ENaC in cell lines and primary epithelial cells, in submerged cultures or grown in air-liquid interface conditions...
April 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28385297/renal-tubular-nhe3-is-required-in-the-maintenance-of-water-and-sodium-chloride-homeostasis
#16
Robert A Fenton, Søren B Poulsen, Samantha de la Mora Chavez, Manoocher Soleimani, Jessica A Dominguez Rieg, Timo Rieg
The sodium/proton exchanger isoform 3 (NHE3) is expressed in the intestine and the kidney, where it facilitates sodium (re)absorption and proton secretion. The importance of NHE3 in the kidney for sodium chloride homeostasis, relative to the intestine, is unknown. Constitutive tubule-specific NHE3 knockout mice (NHE3(loxloxCre)) did not show significant differences compared to control mice in body weight, blood pH or bicarbonate and plasma sodium, potassium, or aldosterone levels. Fluid intake, urinary flow rate, urinary sodium/creatinine, and pH were significantly elevated in NHE3(loxloxCre) mice, while urine osmolality and GFR were significantly lower...
April 3, 2017: Kidney International
https://www.readbyqxmd.com/read/28383056/involvement-of-epithelial-na-channel-in-the-elevated-myogenic-response-in-posterior-cerebral-arteries-from-spontaneously-hypertensive-rats
#17
Soo-Kyoung Choi, Soo-In Yeon, Youngin Kwon, Seonhee Byeon, Young-Ho Lee
Hypertension is characterized by increased peripheral vascular resistance which is related with elevated myogenic response. Recent findings have indicated that epithelial sodium channel (ENaC) is involved in mechanotransduction of the myogenic response. The purpose of this study was to investigate the involvement of ENaC in the elevated myogenic response of posterior cerebral arteries (PCAs) from spontaneously hypertensive rats (SHRs). Sixteen to eighteen weeks old male wistar kyoto rats (WKYs) and SHRs were used in this study...
April 6, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28334404/calcium-homeostasis-modulator-1-like-currents-in-rat-fungiform-taste-cells-expressing-amiloride-sensitive-sodium-currents
#18
Albertino Bigiani
Salt reception by taste cells is still the less understood transduction process occurring in taste buds, the peripheral sensory organs for the detection of food chemicals. Although there is evidence suggesting that the epithelial sodium channel (ENaC) works as sodium receptor, yet it is not clear how salt-detecting cells signal the relevant information to nerve endings. Taste cells responding to sweet, bitter, and umami substances release ATP as neurotransmitter through a nonvesicular mechanism. Three different channel proteins have been proposed as conduit for ATP secretion: pannexin channels, connexin hemichannels, and calcium homeostasis modulator 1 (CALHM1) channels...
May 1, 2017: Chemical Senses
https://www.readbyqxmd.com/read/28334294/an-examination-of-the-role-of-l-glutamate-and-inosine-5-monophosphate-in-hedonic-taste-guided-behavior-by-mice-lacking-the-t1r1-t1r3-receptor
#19
Ginger D Blonde, Alan C Spector
The heterodimeric T1R1 + T1R3 receptor is considered critical for normal signaling of L-glutamate and 5'-ribonucleotides in the oral cavity. However, some taste-guided responsiveness remains in mice lacking one subunit of the receptor, suggesting that other receptors are sufficient to support some behaviors. Here, mice lacking both receptor subunits (KO) and wild-type (WT, both n = 13) mice were tested in a battery of behavioral tests. Mice were trained and tested in gustometers with a concentration series of Maltrin-580, a maltodextrin, in a brief-access test (10-s trials) as a positive control...
June 1, 2017: Chemical Senses
https://www.readbyqxmd.com/read/28289184/renal-tubular-ubiquitin-protein-ligase-nedd4-2-is-required-for-renal-adaptation-during-long-term-potassium-depletion
#20
Lama Al-Qusairi, Denis Basquin, Ankita Roy, Renuga Devi Rajaram, Marc P Maillard, Arohan R Subramanya, Olivier Staub
Adaptation of the organism to potassium (K(+)) deficiency requires precise coordination among organs involved in K(+) homeostasis, including muscle, liver, and kidney. How the latter performs functional and molecular changes to ensure K(+) retention is not well understood. Here, we investigated the role of ubiquitin-protein ligase NEDD4-2, which negatively regulates the epithelial sodium channel (ENaC), Na(+)/Cl(-) cotransporter (NCC), and with no-lysine-kinase 1 (WNK1). After dietary K(+) restriction for 2 weeks, compared with control littermates, inducible renal tubular NEDD4-2 knockout (Nedd4L(Pax8/LC1) ) mice exhibited severe hypokalemia and urinary K(+) wasting...
March 13, 2017: Journal of the American Society of Nephrology: JASN
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