TY - JOUR. T1 - Bumetanide inhibition of the blood-brain barrier Na-K-Cl cotransporter reduces edema formation in the rat middle cerebral artery occlusion model of stroke. AU - ODonnell, Martha E. AU - Tran, Lien. AU - Lam, Tina I.. AU - Liu, Xiao Bo. AU - Anderson, Steven E.. PY - 2004/9. Y1 - 2004/9. N2 - Increased transport of Na+ across an intact blood-brain barrier (BBB) participates in edema formation during the early hours of cerebral ischemia. In previous studies, the authors showed that the BBB Na-K-Cl cotransporter is stimulated by factors present during ischemia, suggesting that the cotransporter may contribute to the increased brain Na+ uptake in edema. The present study was conducted to determine (1) whether the Na-K-Cl cotransporter is located in the luminal membrane of the BBB, and (2) whether inhibition of the BBB cotransporter reduces brain edema formation. Perfusion-fixed rat brains were examined for cotransporter distribution by immunoelectron microscopy. Cerebral edema was ...
Mutations in the WNK [with no lysine (K) kinase] family instigate hypertension and pain perception disorders. Of the four WNK isoforms, much of the focus has been on WNK1, which is activated in response to osmotic stress by phosphorylation of its T-loop residue (Ser382). WNK isoforms phosphorylate and activate the related SPAK (SPS1-related proline/alanine-rich kinase) and OSR1 (oxidative stress-responsive kinase 1) protein kinases. In the present study, we first describe the generation of double-knockin ES (embryonic stem) cells, where SPAK and OSR1 cannot be activated by WNK1. We establish that NKCC1 (Na+/K+/2Cl- co-transporter 1), a proposed target of the WNK pathway, is not phosphorylated or activated in a knockin that is deficient in SPAK/OSR1 activity. We also observe that activity of WNK1 and WNK3 are markedly elevated in the knockin cells, demonstrating that SPAK/OSR1 significantly influences WNK activity. Phosphorylation of another regulatory serine residue, Ser1261, in WNK1 is ...
p>The checksum is a form of redundancy check that is calculated from the sequence. It is useful for tracking sequence updates.,/p> ,p>It should be noted that while, in theory, two different sequences could have the same checksum value, the likelihood that this would happen is extremely low.,/p> ,p>However UniProtKB may contain entries with identical sequences in case of multiple genes (paralogs).,/p> ,p>The checksum is computed as the sequence 64-bit Cyclic Redundancy Check value (CRC64) using the generator polynomial: x,sup>64,/sup> + x,sup>4,/sup> + x,sup>3,/sup> + x + 1. The algorithm is described in the ISO 3309 standard. ,/p> ,p class="publication">Press W.H., Flannery B.P., Teukolsky S.A. and Vetterling W.T.,br /> ,strong>Cyclic redundancy and other checksums,/strong>,br /> ,a href="http://www.nrbook.com/b/bookcpdf.php">Numerical recipes in C 2nd ed., pp896-902, Cambridge University Press (1993),/a>),/p> Checksum:i ...
Sigma-Aldrich offers abstracts and full-text articles by [Eleni Roussa, Jan Manuel Speer, Ilona Chudotvorova, Shokoufeh Khakipoor, Sergei Smirnov, Claudio Rivera, Kerstin Krieglstein].
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NKCC (Na-K-Cl cotransporter) is a protein that aids in the active transport of sodium, potassium, and chloride into and out of cells. There are two varieties of this membrane transport protein, NKCC1 and NKCC2, however these are encoded by two different genes (SLC12A2 and SLC12A1 respectively) and are not isoforms. Two isoforms of the NKCC1/Slc12a2 gene result from keeping (isoform 1) or skipping (isoform 2) exon 21 in the final gene product. NKCC1 is widely distributed throughout the body; it has important functions in organs that secrete fluids. NKCC2 is found specifically in the kidney, where it serves to extract sodium, potassium, and chloride from the urine so that they can be reabsorbed into the blood. NKCC proteins are membrane transport proteins that transport sodium (Na), potassium (K), and chloride (Cl) ions across the cell membrane. Because they move each solute in the same direction, NKCC proteins are considered symporters. ...
Inhibition of Na(+)-K(+)-Cl(-) cotransporter during focal cerebral ischemia decreases edema and neuronal damage. - Yiping Yan, Robert J Dempsey, Andreas Flemmer, Biff Forbush, Dandan Sun
Heterocyclic compounds of a ring with SULFUR and two NITROGEN atoms fused to a BENZENE ring. Members inhibit SODIUM-POTASSIUM-CHLORIDE SYMPORTERS and are used as DIURETICS ...
The cation-chloride cotransporters Na+-K+-2Cl--1 (NKCC1) and K+-2Cl--2 (KCC2) critically regulate neuronal responses to gamma-aminobutyric acid (GABA). NKCC1 renders GABA excitatory in immature neurons while expression of KCC2 signals GABA maturation to its inhibitory role. Imbalances in NKCC1/KCC2 alter GABA neurotransmission, which may contribute to hyperexcitability and blunted inhibition in neurocircuitry after neonatal exposure to anesthesia. Thus, we hypothesized that anesthetics may dysregulate NKCC1 and/or KCC2 in developing brain. We exposed postnatal day (PND) 7 mice to sevoflurane or carrier gases and assessed NKCC1 and KCC2 expression across three brain regions 6 h and 24 h after initial exposure. To test differences in behavior, we challenged pups receiving sevoflurane or carrier gases on PND7 with propofol on PND8 and recorded parameters of anesthesia induction and maintenance. Sevoflurane exposure increased cortical NKCC1 at 6 h (p = 0.03) and decreased cortical and hippocampal ...
Precise homoeostasis of the intracellular concentration of Cl -. is achieved via the co-ordinated activities of the Cl -. influx and efflux. We demonstrate that the WNK (WNK lysine-deficient protein kinase)-activated SPAK (SPS1-related proline/alanine-rich kinase)/OSR1 (oxidative stress-responsive kinase 1) knownto directly phosphorylate and stimulate the N[K]CCs (Na + -K +. ion co-transporters), also promote inhibition of the KCCs (K + -Cl -. co-transporters) by directly phosphorylating a recently described C-terminal threonine residue conserved in allKCCisoforms [Site-2 (Thr 1048 )]. First, we demonstrate that SPAK and OSR1, in the presence of theMO25 regulatory subunit, robustly phosphorylates allKCC isoforms at Site-2 in vitro. Secondly, STOCK1S-50699, a WNK pathway inhibitor, suppresses SPAK/OSR1 activation and KCC3ASite-2 phosphorylationwith similar efficiency. Thirdly, in ES (embryonic stem) cells lacking SPAK/OSR1 activity, endogenous phosphorylation of KCC isoforms at Site-2 is ...
The anion dependence of [3H]bumetanide binding and 22Na+ transport by the rabbit parotid Na(+)-K(+)-2Cl- co-transporter was studied in acinar basolateral membrane vesicles (BLMVs). Cl-, Br- and NO3- have a biphasic effect on binding consistent with the presence of two anion sites associated with the bumetanide binding event, a high-affinity stimulatory site and a lower-affinity inhibitory site. We show that formate shares only the stimulatory site and SO4(2-) only the inhibitory site. The initial rate of [3H]bumetanide binding was stimulated by formate or low [Cl-] and inhibited by SO4(2-) or high [Cl-], but the rate of [3H]bumetanide dissociation was not affected by the presence of these anions in the dissociation medium. However, when [3H]bumetanide was bound to BLMVs in the presence of formate its rate of dissociation was more than four times faster than when binding took place in the presence of Cl-. These observations indicate that the binding of bumetanide and the stimulatory anion are ...
Fluid and HCO3- secretion are fundamental functions of epithelia and determine bodily fluid volume and ionic composition, among other things. Secretion of ductal fluid and HCO3- in secretory glands is fueled by Na+/HCO3- cotransport mediated by basolateral solute carrier family 4 member 4 (NBCe1-B) and by Cl-/HCO3- exchange mediated by luminal solute carrier family 26, member 6 (Slc26a6) and CFTR. However, the mechanisms governing ductal secretion are not known. Here, we have shown that pancreatic ductal secretion in mice is suppressed by silencing of the NBCe1-B/CFTR activator inositol-1,4,5-trisphosphate (IP3) receptor-binding protein released with IP3 (IRBIT) and by inhibition of protein phosphatase 1 (PP1). In contrast, silencing the with-no-lysine (WNK) kinases and Ste20-related proline/alanine-rich kinase (SPAK) increased secretion. Molecular analysis revealed that the WNK kinases acted as scaffolds to recruit SPAK, which phosphorylated CFTR and NBCe1-B, reducing their cell surface ...
The Na-K-Cl cotransporter (NKCC) is present in most animal cells where it functions in cell volume homeostasis and epithelial salt transport. We developed six monoclonal antibodies (designated T4, T8, T9, T10, T12, and T14) against a fusion protein fragment encompassing the carboxy-terminal 310 amin …
Mammalian Ste20-like proline/alanine-rich kinase (SPAK) and oxidative stress-responsive 1 (OSR1) kinases phosphorylate and regulate cation-coupled Cl? cotransporter activity in response to cell quantity changes. activity of CLH-3b expressed in worm oocytes endogenously. Earlier yeast 2-cross research suggested that ERK kinases may function of GCK-3 upstream. Meclizine 2HCl Pharmacological inhibition of ERK signaling disrupted CLH-3b activity in HEK cells inside a GCK-3-reliant Meclizine 2HCl way. RNAi silencing from the ERK kinase MPK-1 or the ERK phosphorylating/activating kinase MEK-2 constitutively triggered native CLH-3b. MEK-2 and MPK-1 play important roles in regulating the meiotic cell cycle in oocytes. Cell cycle-dependent changes in MPK-1 correlate with the pattern of CLH-3b activation observed during oocyte meiotic maturation. We postulate that MEK-2/MPK-1 functions upstream from GCK-3 to regulate its activity during cell volume and meiotic cell cycle changes. oocyte is activated by ...
Mammalian Ste20-like proline/alanine-rich kinase (SPAK) and oxidative stress-responsive 1 (OSR1) kinases phosphorylate and regulate cation-coupled Cl? cotransporter activity in response to cell quantity changes. activity of CLH-3b expressed in worm oocytes endogenously. Earlier yeast 2-cross research suggested that ERK kinases may function of GCK-3 upstream. Meclizine 2HCl Pharmacological inhibition of ERK signaling disrupted CLH-3b activity in HEK cells inside a GCK-3-reliant Meclizine 2HCl way. RNAi silencing from the ERK kinase MPK-1 or the ERK phosphorylating/activating kinase MEK-2 constitutively triggered native CLH-3b. MEK-2 and MPK-1 play important roles in regulating the meiotic cell cycle in oocytes. Cell cycle-dependent changes in MPK-1 correlate with the pattern of CLH-3b activation observed during oocyte meiotic maturation. We postulate that MEK-2/MPK-1 functions upstream from GCK-3 to regulate its activity during cell volume and meiotic cell cycle changes. oocyte is activated by ...
GABA depolarizes and excites central neurons during early development, becoming inhibitory and hyperpolarizing with maturation. This
The thiazide-sensitive Na+:Cl- cotransporter is the major salt transport pathway in the distal convoluted tubule of the kidney, and a role of this cotransporter in blood pressure homeostasis has been defined by physiological studies on pressure natriuresis and by its involvement in monogenic diseases that feature arterial hypotension or hypertension. Data base analysis revealed that 135 single nucleotide polymorphisms along the human SLC12A3 gene that encodes the Na+:Cl- cotransporter have been reported. Eight are located within the coding region, and one results in a single amino acid change; the residue glycine at the position 264 is changed to alanine (G264A). This residue is located within the fourth transmembrane domain of the predicted structure. Because Gly-264 is a highly conserved residue, we studied the functional properties of this polymorphism by using in vitro mutagenesis and the heterologous expression system in Xenopus laevis oocytes. G264A resulted in a significant and ...
Prenatally programmed hypertension induced by maternal protein restriction is associated with increased expression of the renal tubular Na+/K+/2Cl− co-transporter (NKCC2) and the Na+/Cl− co-transporter (NCC). This has led to the suggestion that renal Na+ retention contributes to the development of hypertension in the LP rat (offspring exposed to a maternal low-protein diet in utero). However, this hypothesis has not been tested in vivo. Renal clearance measurements in hypertensive 4-week-old male and female LP rats showed that, although the glomerular filtration rate remained unaltered, urine flow (P,0.01) and urinary Na+ excretion rates (1.6±0.3 and 3.0±0.4 μmol·min−1·100 g−1 of body weight in control male and LP male respectively; P,0.001) were increased. Na+ excretion was positively correlated with mean arterial pressure in both males (P,0.01) and females (P,0.05), but neither the slope nor the intercept differed between control and LP rats. Fractional excretion of Na+ was ...
The N-K-Cl cotransporters (NKCCs) mediate the coupled, electroneutral movement of Na(+) , K(+) and Cl(-) ions across cell membranes. There are two isoforms of this cation co-transporter, NKCC1 and NKCC2. NKCC2 is expressed primarily in the kidney and is the target of diuretics such as bumetanide. Bumetanide was discovered by screening ∼5000 3-amino-5-sulfamoylbenzoic acid derivatives, long before NKCC2 was identified in the kidney. Therefore, structure-activity studies on effects of bumetanide derivatives on NKCC2 are not available. In this study, the effect of a series of diuretically active bumetanide derivatives was investigated on human NKCC2 variant A (hNKCC2A) expressed in Xenopus laevis oocytes. Bumetanide blocked hNKCC2A transport with an IC50 of 4 μM. There was good correlation between the diuretic potency of bumetanide and its derivatives in dogs and their inhibition of hNKCC2A (r(2) = 0.817; P , 0.01). Replacement of the carboxylic group of bumetanide by a non-ionic residue, for ...
Intestinal Na-Pi-IIb cotransporter likely plays a major role in the regulation of Pi homeostasis. Although Pi homeostasis is a tightly controlled process, lower plasma Pi levels have been observed in old age and in the case of chronic GC treatment (5, 30, 38). In both cases, decreased renal Pi absorption was reported and was associated with reduced Na-Pi-IIa expression, (1, 18,43). To date, the downregulation of intestinal Piabsorption has not been investigated with respect to possible alterations in Na-Pi-IIb cotransporter expression, although reduced intestinal Pi absorption has been reported in old animals. We hypothesized that the age-related and GC-induced reductions of total intestinal Na-Pi transport would correlate with decreases in intestinal Na-Pi-IIb expression. Therefore, the present work focused on the ontogeny of intestinal Na-Pi uptake and Na-Pi-IIb expression at distinct periods throughout the lifespan and how pharmacological doses of GCs affect the same processes.. In laboratory ...
Author: Nalbant, P. et al.; Genre: Other; Published in Print: 1999; Title: PDZ-domain interaction of the Na/P-i cotransporter type II
The with-no-lysine (K) kinases, WNK1 and WNK4, are key regulators of blood pressure. Their mutations lead to familial hyperkalemic hypertension (FHHt), associated with an activation of the Na-Cl cotransporter (NCC). Although it is clear that WNK4 mutants activate NCC via Ste20 proline-alanine-rich kinase, the mechanisms responsible for WNK1-related FHHt and alterations in NCC activity are not as clear. We tested whether WNK1 modulates NCC through WNK4, as predicted by some models, by crossing our recently developed WNK1-FHHt mice (WNK1+/FHHt) with WNK4−/− mice. Surprisingly, the activated NCC, hypertension, and hyperkalemia of WNK1+/FHHt mice remain in the absence of WNK4. We demonstrate that WNK1 powerfully stimulates NCC in a WNK4-independent and Ste20 proline-alanine-rich kinase-dependent manner. Moreover, WNK4 decreases the WNK1 and WNK3-mediated activation of NCC. Finally, the formation of oligomers of WNK kinases through their C-terminal coiled-coil domain is essential for their ...
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Inhibition of Jak/STAT Signaling Reduces the Activation of Pancreatic Stellate Cells In Vitro and Limits Cerulein-Induced Chronic Pancreatitis In Vivo Investigators utilized primary and immortalized pancreatic stellate cells obtained from mice and patients with chronic pancreatitis (CP) or pancreatic cancer to examine the effect of Jak/STAT and MAPK pathway inhibition in vitro. The well-characterized cerulein model of CP was used to assess the therapeutic efficacy of Jak1/2 inhibition in vivo. [Sci Rep] Full Article The Neuronal K+Cl− Co-Transporter 2 (Slc12a5) Modulates Insulin Secretion Using molecular cloning, RT-PCR, Western blotting, immunolocalization and in vitro functional assays, researchers established that the "neuron-specific" K+Cl− co-transporter 2 (Slc12a5) is expressed in several endocrine cells of the pancreatic islet, including glucagon secreting α-cells, but particularly in insulin-secreting β-cells, where they provide evidence for its role in the insulin secretory ...
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Although the physiological functions of KCC2 in chicken cardiomyocytes remain poorly understood, K+-Cl− cotransporters have been implicated in the regulation of cell volume, intracellular [Cl−], and extracellular [K+] (19, 31, 32, 38). In addition to potential roles in regulating cell volume and extracellular [K+] in cardiomyocytes, KCC2 could contribute importantly to the control of intracellular [Cl−]. Analogous to its function in mature central neurons, we postulate that KCC2 in cardiomyocytes could serve as a Cl− extrusion pathway that helps maintain the Cl− electrochemical gradient needed for proper anion channel function in cardiomyocytes. Because KCC2a exhibits a regulatory site within its first exon (SPAK/OSR1 binding motif), the exclusive expression of KCC2a in chicken cardiomyocytes could permit differential regulation in cardiomyocytes vs. KCC2b, which predominates in central neurons. Cardiomyocytes do exhibit some characteristics with regard to Cl− homeostasis that are ...
Polyclonal antibody for NKCC2/SLC12A1 detection. Host: Rabbit.Size: 100μg/vial. Tested applications: IHC-P. Reactive species: Human. NKCC2/SLC12A1 information: Molecular Weight: 121450 MW; Subcellular Localization: Membrane; Multi-pass membrane protein; T
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TY - JOUR. T1 - Cyclosporine reduces basolateral, but not apical, nitric oxide secretion in medullary thick ascending limb cells. AU - Wu, M. S.. AU - Bens, M.. AU - Yu, H. M.. AU - Vandewalle, A.. PY - 2000. Y1 - 2000. N2 - Cyclosporine (CsA) reduces nitric oxide (NO) production in medullary thick ascending limb (mTAL) cells. We postulated that CsA affected NO secretion in a vectorial manner in polarized renal epithelial cells. The experiments were performed in a model of mTAL subcultured cells. The expression of iNOS in mTAL cells was confirmed by RT-PCR. The cells were grown on a non-permeable filter. Nitrite was measured by the modified Griess method. Transepithelial resistance was measured to ensure the integrity of the tight junction. CsA (100 ng/ml) reduced NO production by 22% in mTAL cells. The inhibitory effect was limited to the basolateral side (control: 165 ± 11; plus CsA: 93 ± 17 nM/106 cells, P ,0.001) without affecting apical NO secretion. The transepithelial resistance through ...
Bartter syndrome is a rare inherited defect in the thick ascending limb of the loop of Henle. It is characterized by low potassium levels (hypokalemia), increased blood pH (alkalosis), and normal to low blood pressure. There are two types of Bartter syndrome: neonatal and classic. A closely associated disorder, Gitelman syndrome, is milder than both subtypes of Bartter syndrome. In 90% of cases, neonatal Bartter syndrome is seen between 24 and 30 weeks of gestation with excess amniotic fluid (polyhydramnios). After birth, the infant is seen to urinate and drink excessively (polyuria, and polydipsia, respectively). Life-threatening dehydration may result if the infant does not receive adequate fluids. About 85% of infants dispose of excess amounts of calcium in the urine (hypercalciuria) and kidneys (nephrocalcinosis), which may lead to kidney stones. In rare occasions, the infant may progress to renal failure. Patients with classic Bartter syndrome may have symptoms in the first two years of ...
Bartter syndrome is a rare inherited kidney disorder in the thick ascending limb of the loop of Henle. It is characterized by low potassium levels (hypokalemia), increased blood pH (alkalosis), and normal to low blood pressure. There are two types of Bartter syndrome: neonatal and classic. A closely associated disorder, Gitelman syndrome, is milder than both subtypes of Bartter syndrome.Wikipedia Bartter and Gitelman syndromes can be divided into different subtypes based on the genes involved 10.1159/000076752: ...
To treat Bartter Syndrome, it is imperative to maintain adequate potassium levels in the body. Infant suffering with Neonatal Bartter Syndrome urinate (polyuria) and drink (polydipsia) excessive fluid. Know its treatment, prognosis, causes and symptoms.
Vasoconstriction is a signature physiological action of angiotensin II (AngII) acting via AT1 receptors (AT1R). In order to define the contribution of AT1R in vascular smooth muscle cells (VSMCs) to BP control, we generated mice with cell-specific deletion of AT1AR from VSMCs (SMKOs) using Cre-loxp technology. Baseline BP was reduced by ~7 mmHg and responses to AngII-induced hypertension were significantly blunted by in SMKO mice compared to controls (16 vs. 30 mm Hg change in BP from baseline after 4 wks AngII, P,0.02). Baseline renal blood flow (RBF) was higher, and renal vasoconstriction after Ang II was impaired in SMKOs. Moreover, SMKO mice displayed Na+ sensitivity and exaggerated natriuresis during chronic AngII infusion. To investigate the mechanism of the lower baseline BP and the enhanced natriuresis during AngII infusion (1000ng/kg/min for 5 days), we measured a panel of key Na+ transporters in the kidney by immunoblot. Baseline measurements in SMKO vs. controls detected reductions in ...
530(Pt 3), 359-66. The Na+-H+ exchanger NHE3 and the thiazide-sensitive Na+-Cl- cotransporter NCC are the major apical sodium transporters in the proximal convoluted tubule and the distal convoluted tubule of the kidney, respectively. We investigated the mechanism of compensation that allows maintenance of sodium balance in NHE3 knockout mice and in NCC knockout mice. We used a so-called targeted proteomics approach, which profiles the entire renal tubule with regard to changes in Na+ transporter and aquaporin abundance in response to the gene deletions. Specific antibodies to the Na+ transporters and aquaporins expressed along the nephron were utilized to determine the relative abundance of each transporter. Semiquantitative immunoblotting was used which gives an estimate of the percentage change in abundance of each transporter in knockout compared with wild-type mice. In NHE3 knockout mice three changes were identified which could compensate for the loss of NHE3-mediated sodium absorption. ...
Denoyer, Delphine, Perek, Nathalie, Le Jeune, Nathalie, Frere, Delphine and Dubois, Francis 2004, Evidence that 99mTc-(V)-DMSA uptake is mediated by NaPi cotransporter type III in tumour cell lines, European journal of nuclear medicine and molecular imaging, vol. 31, no. 1, pp. 77-84, doi: 10.1007/s00259-003-1334-7. ...
The balance between salt excretion and absorption in the kidney tubules is a major determinant of vascular volume homeostasis and systemic blood pressure. The k...
Many theories of neural processing focus quite rightly on computational and information processing concerns. While this is entirely sensible, the brain is not an abstract computational device, it generates heat, it is noisy, and requires a high energy-density diet to power it. Much of my work focuses on the role of such biophysical factors. In a series of studies which use simple neural networks/Bayesian models, I and colleagues have found that the remarkably simple notion of do work, whilst being energy efficient can explain multiple properties of the neural organisation of early sensory systems. 27/04/10 11:00 - 12:00. ANC Seminar: Michael Daw (Host: Mark van Rossum). "Coordinated development of feedforward inhibition in neonatal cortex". Early changes in the expression of neuronal chloride transporters result in a developmental switch at GABAergic synapses from depolarising transmission to the hyperpolarising transmission which is typical in the adult brain. Studies in a number of brain ...
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Barkla,B.J. Pantoja,O. 2011. Plasma Membrane and Abiotic Stress en: Murphy,A. Plant Plasma Membrane, Plant Cell Monographs. Springer. pags. 457-470 Barkla,B.J. Vera-Estrella,R. Balderas,E. Pantoja,O. 2008. Mecanismos de tolerancia a la salinidad en plantas en: Lopez-Munguia,A. Una ventana al quehacer cient fico. Instituto de Biotecnolog a de la UNAM 25 aniversario, cap 23. Mexico, D.F.. UNAM. pags. 263-272 Pantoja,O. Barkla,B.J. Vera-Estrella,R. 2000. Ion channels and ion co-transporters in the tonoplast en: Rogers,J.C. Vacuolar Compartments. Sheffield Academic Press. pags. 199-220 ...
Synonyms : Desbutylbumetanide; 3-Amino-4-phenoxy-5-sulfamoylbenzoic acid; 3-Amino-5-(aminosulfonyl)-4-phenoxy-benzoic Acid; USP Bumetanide Related Compound A, Bumetanide impurity B (EP ...
The IUPHAR/BPS Guide to Pharmacology. bumetanide ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
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44339119 -OEChem-10101305022D 37 39 0 0 0 0 0 0 0999 V2000 8.0785 2.9476 0.0000 Cl 0 0 0 0 0 0 0 0 0 0 0 0 8.9962 0.3922 0.0000 N 0 0 0 0 0 0 0 0 0 0 0 0 8.0785 -1.1215 0.0000 N 0 0 0 0 0 0 0 0 0 0 0 0 8.9271 -2.6315 0.0000 N 0 0 0 0 0 0 0 0 0 0 0 0 9.8105 -1.1416 0.0000 N 0 0 0 0 0 0 0 0 0 0 0 0 5.4641 0.4131 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 7.1962 0.4131 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 7.1962 1.4130 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 4.5981 -0.0869 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 6.3301 -0.0869 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 5.4641 1.4130 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 6.3301 1.9130 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 8.0901 -0.1216 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 3.7320 0.4131 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 4.5981 -1.0870 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 8.0901 1.9477 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 2.8660 -1.0870 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 2.8660 -0.0869 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 3.7320 -1.5870 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 8.9962 1.4339 0.0000 C 0 0 0 0 0 0 0 0 0 0 0 0 ...
Studies of unidirectional Cl-, Na+, and K+ effluxes were performed on isolated, internally dialyzed squid giant axons. The studies were designed to determine whether the coupled Na/K/Cl co-transporter previously identified as mediating influxes (Russell. 1983. Journal of General Physiology. 81:909-925) could also mediate the reverse fluxes (effluxes). We found that 10 microM bumetanide blocked 7-8 pmol/cm2 X s of Cl- efflux from axons containing ATP, Na+, and K+. However, if any one of these solutes was removed from the internal dialysis fluid, Cl- efflux was reduced by 7-8 pmol/cm2 X s and the remainder was insensitive to bumetanide. About 5 pmol/cm2 X s of Na+ efflux was inhibited by 10 microM bumetanide in the continuous presence of 10(-5) M ouabain and 10(-7) M tetrodotoxin if Cl-, K+, and ATP were all present in the internal dialysis fluid. However, the omission of Cl- or K+ or ATP reduced the Na+ efflux, leaving it bumetanide insensitive. K+ efflux had to be studied under voltage-clamp ...
Bartter syndrome (BS) type 1, also referred to antenatal BS, is a genetic tubulopathy with hypokalemic metabolic alkalosis and prenatal onset of polyuria leading to polyhydramnios. It has been shown that BS type 1 is caused by mutations in the SLC12A1 gene encoding bumetanide-sensitive Na-K-2Cl (-) …
NKCC1 Antagonist Reduces Seizures in Rodent Models. Volodymyr I. Dzhala, Kishore V. Kuchibhotla, Joseph C. Glykys, Kristopher T. Kahle, Waldemar B. Swiercz, et al.. (see pages 11745-11761). During development, GABA is excitatory because relatively high expression of the neuronal sodium-potassium-chloride cotransporter (NKCC1) raises intracellular chloride concentrations, making the reversal potential for GABA receptors (EGABA) more depolarized than resting membrane potential (Vm). Although EGABA is normally hyperpolarized relative to Vm in mature neurons, seizures can depolarize EGABA, thus reducing or reversing inhibitory currents and increasing the likelihood of future seizures. Dzhala et al. found that kainic acid, GABA receptor antagonists, or reduced extracellular magnesium concentration caused recurrent seizures that progressively increased in frequency in intact neonatal rodent hippocampi. Although GABA agonist had a net inhibitory effect after the first seizure, this effect was ...
Subjects will be examined on two examination days. 4 days prior to each examination day subjects are treated with either atorvastatin or placebo. During treatment periods subject are given a standardized diet.. On the examination days subject are given L-NMMA(L-NG-monomethyl Arginine citrate), a NO inhibitor, 6 mg bolus infusion followed by continuous 4 mg/kg/hr infusion for 1 hour. Renal function, central hemodynamic and vasoactive hormones are evaluated prior, during and after L-NMMA infusion.. Renal function is measured by renal clearance of 51Cr-EDTA and urinary sodium, potassium and albumin concentration. Urinary excretion of protein from sodium channels such as the NaCl cotransporter (NCC), the Na-K-Cl cotransporter (NKCC) and the epithelial sodium channel (ENaC)will be measured to evaluate channel activity in the nephron.. Central blood pressure, pulse wave analysis, and augmentation index are measured using SphygmoCor® from Atcor.. The vasoactive hormones aldosterone, renin, angiotensin ...
Several dozen mutations in the KCNJ1 gene have been identified in people with Bartter syndrome type II. This form of the disorder causes severe or life-threatening health problems that become apparent before or soon after birth.. Some of the KCNJ1 gene mutations responsible for Bartter syndrome change single protein building blocks (amino acids) in the ROMK protein. These mutations prevent the protein from reaching the cell membrane or alter the channels ability to transport potassium ions. Other mutations in the KCNJ1 gene delete amino acids from the protein or lead to the production of an abnormally short, nonfunctional version of ROMK.. A loss of functional ROMK affects the normal activity of the NKCC2 protein, preventing it from transporting ions into kidney cells. As a result, the kidneys cannot reabsorb salt normally and excess salt is lost through the urine (salt wasting). The abnormal salt loss disrupts the normal balance of sodium, potassium, and other ions in the body. These ...