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https://www.readbyqxmd.com/read/27861335/response-of-fibroblast-growth-factor-23-to-volume-interventions-in-arterial-hypertension-and-diabetic-nephropathy
#1
Jelmer K Humalda, Sarah Seiler-Muler, Arjan J Kwakernaak, Marc G Vervloet, Gerjan Navis, Danilo Fliser, Gunnar H Heine, Martin H de Borst
Fibroblast growth factor 23 (FGF-23) rises progressively in chronic kidney disease and is associated with adverse cardiovascular outcomes. FGF-23 putatively induces volume retention by upregulating the sodium-chloride cotransporter (NCC). We studied whether, conversely, interventions in volume status affect FGF-23 concentrations.We performed a post hoc analysis of 1) a prospective saline infusion study with 12 patients with arterial hypertension who received 2 L of isotonic saline over 4 hours, and 2) a randomized controlled trial with 45 diabetic nephropathy (DN) patients on background angiotensin-converting enzyme -inhibition (ACEi), who underwent 4 6-week treatment periods with add-on hydrochlorothiazide (HCT) or placebo, combined with regular sodium (RS) or low sodium (LS) diet in a cross-over design...
November 2016: Medicine (Baltimore)
https://www.readbyqxmd.com/read/27815594/wnk-signalling-pathways-in-blood-pressure-regulation
#2
REVIEW
Meena Murthy, Thimo Kurz, Kevin M O'Shaughnessy
Hypertension (high blood pressure) is a major public health problem affecting more than a billion people worldwide with complications, including stroke, heart failure and kidney failure. The regulation of blood pressure is multifactorial reflecting genetic susceptibility, in utero environment and external factors such as obesity and salt intake. In keeping with Arthur Guyton's hypothesis, the kidney plays a key role in blood pressure control and data from clinical studies; physiology and genetics have shown that hypertension is driven a failure of the kidney to excrete excess salt at normal levels of blood pressure...
November 4, 2016: Cellular and Molecular Life Sciences: CMLS
https://www.readbyqxmd.com/read/27789743/channel-transporter-complexes-an-emerging-theme-in-cell-signaling
#3
Geoffrey W Abbott
In a recent edition of Biochemical Journal, Mistry and colleagues described the discovery of a novel protein complex, formed from the epithelial sodium channel (ENaC) and the sodium chloride cotransporter (NCC) [Biochem. J. (2016) Hoover, S.R]. The importance of these two proteins in the regulation of salt balance and blood pressure has long been known, as has their overlapping expression in the distal convoluted tubule of the kidney. The new study by Mistry et al. now demonstrates their physical interaction in the kidney and when heterologously co-expressed...
November 1, 2016: Biochemical Journal
https://www.readbyqxmd.com/read/27760769/a-small-molecule-screening-to-detect-potential-therapeutic-targets-in-human-podocytes
#4
Eugen Widmeier, Weizhen Tan, Merlin Airik, Friedhelm Hildebrandt
INTRODUCTION: Steroid-resistant nephrotic syndrome (SRNS) inevitably progresses to end-stage kidney disease, requiring dialysis or transplantation for survival. However, treatment modalities and drug discovery remain limited. Mutations in over 30 genes have been discovered as monogenic causes of SRNS. Most of these genes are predominantly expressed in the glomerular epithelial cell, the podocyte, placing it at the center of the pathogenesis of SRNS. Podocyte migration rate (PMR) represents a relevant intermediate phenotype of disease in monogenic causes of SRNS...
October 19, 2016: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/27754152/os-29-04-sympathetic-nervous-system-regulation-of-the-renal-ncc-and-blood-pressure-during-high-dietary-salt-intake
#5
Richard Wainford, Kathryn Walsh
OBJECTIVE: These studies tested the hypothesis that the SNS release of norepinephrine modulates NCC activity via a WNK1 mechanism to contribute to the pathophysiology of salt-sensitive hypertension in rats. DESIGN AND METHOD: Male Sprague-Dawley (SD) rats receiving a continuous s.c. saline or NE (600 ng/min) infusion or naïve Dahl Salt-Resistant (DSR) and Dahl Salt-Sensitive (DSS) rats were fed a 0.6% (NS) or 8% NaCl (HS) diet for 14 or 21 days respectively (N = 6/group)...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27753890/ish-nia-os-05-interleukin-6-transactivation-of-the-mineralocorticoid-receptor
#6
Brandi Wynne, Trinity Kronk, Otor Al-Khalili, Benjamin Ko, Franziska Theilig, Douglas Eaton, Robert Hoover
OBJECTIVE: Hypertension is characterized by increased sodium reabsorption along the aldosterone-sensitive distal nephron (ASDN) and systemic inflammation. Interleukin-6 (IL-6) is a possible mediator, signaling via the transmembrane IL-6 receptor alpha (IL-6Rα); however, whether IL-6Rα is present in the distal convoluted tubule (DCT) is unknown. Increased sodium reabsorption is not always correlated with increased aldosterone (Aldo). Thus, understanding how Aldo-independent sodium reabsorption occurs is critical...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27733368/long-term-aldosterone-administration-increases-renal-na-cl-cotransporter-abundance-in-late-distal-convoluted-tubule
#7
Søren Brandt Poulsen, Birgitte M Christensen
Renal Na+-Cl- cotransporter (NCC) is expressed in early distal convoluted tubule (DCT) 1 and late DCT (DCT2). NCC activity can be stimulated by aldosterone, and the mechanism is assumed to depend on the enzyme, 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which inactivates glucocorticoids that would otherwise occupy aldosterone receptors. Because 11β-HSD2 in rat may only be abundantly expressed in DCT2 cells and not in DCT1 cells, it has been speculated that aldosterone specifically stimulates NCC activity in DCT2 cells...
October 12, 2016: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/27707706/solute-transport-and-oxygen-consumption-along-the-nephrons-effects-of-na-transport-inhibitors
#8
Anita T Layton, Kamel Laghmani, Volker Vallon, Aurélie Edwards
Sodium and its associated anions are the major determinant of extracellular fluid volume, and the reabsorption of Na(+) by the kidney plays a crucial role in long-term blood pressure control. The goal of this study was to investigate the extent to which inhibitors of transepithelial Na(+) transport (TNa) along the nephron alter urinary solute excretion and TNa efficiency and how those effects may vary along different nephron segments. To accomplish that goal, we used the multinephron model developed in the companion study (28)...
December 1, 2016: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/27643236/ish-nia-os-05-interleukin-6-transactivation-of-the-mineralocorticoid-receptor
#9
Brandi Wynne, Trinity Kronk, Otor Al-Khalili, Benjamin Ko, Franziska Theilig, Douglas Eaton, Robert Hoover
OBJECTIVE: Hypertension is characterized by increased sodium reabsorption along the aldosterone-sensitive distal nephron (ASDN) and systemic inflammation. Interleukin-6 (IL-6) is a possible mediator, signaling via the transmembrane IL-6 receptor alpha (IL-6Rα); however, whether IL-6Rα is present in the distal convoluted tubule (DCT) is unknown. Increased sodium reabsorption is not always correlated with increased aldosterone (Aldo). Thus, understanding how Aldo-independent sodium reabsorption occurs is critical...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27643082/os-29-04-sympathetic-nervous-system-regulation-of-the-renal-ncc-and-blood-pressure-during-high-dietary-salt-intake
#10
Richard Wainford, Kathryn Walsh
OBJECTIVE: These studies tested the hypothesis that the SNS release of norepinephrine modulates NCC activity via a WNK1 mechanism to contribute to the pathophysiology of salt-sensitive hypertension in rats. DESIGN AND METHOD: Male Sprague-Dawley (SD) rats receiving a continuous s.c. saline or NE (600 ng/min) infusion or naïve Dahl Salt-Resistant (DSR) and Dahl Salt-Sensitive (DSS) rats were fed a 0.6% (NS) or 8% NaCl (HS) diet for 14 or 21 days respectively (N = 6/group)...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27622885/fgf23-klotho-signaling-axis-in-the-kidney
#11
Reinhold G Erben, Olena Andrukhova
Fibroblast growth factor-23 (FGF23) is a bone-derived hormone protecting against the potentially deleterious effects of hyperphosphatemia by suppression of phosphate reabsorption and of active vitamin D hormone synthesis in the kidney. The kidney is one of the main target organs of FGF23 signaling. The purpose of this review is to highlight the recent advances in the area of FGF23-Klotho signaling in the kidney. During recent years, it has become clear that FGF23 acts independently on proximal and distal tubular epithelium...
September 10, 2016: Bone
https://www.readbyqxmd.com/read/27587391/the-european-eel-ncc%C3%AE-gene-encodes-a-thiazide-resistant-na-cl-cotransporter
#12
Erika Moreno, Consuelo Plata, Alejandro Rodríguez-Gama, Eduardo R Argaiz, Norma Vázquez, Karla Leyva-Ríos, León Islas, Christopher Cutler, Diana Pacheco-Alvarez, Adriana Mercado, Raquel Cariño-Cortés, María Castañeda-Bueno, Gerardo Gamba
The thiazide-sensitive Na-Cl cotransporter (NCC) is the major pathway for salt reabsorption in the mammalian distal convoluted tubule. NCC plays a key role in the regulation of blood pressure. Its inhibition with thiazides constitutes the primary baseline therapy for arterial hypertension. However, the thiazide-binding site in NCC is unknown. Mammals have only one gene encoding for NCC. The eel, however, contains a duplicate gene. NCCα is an ortholog of mammalian NCC and is expressed in the kidney. NCCβ is present in the apical membrane of the rectum...
October 21, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27582101/a-fate-mapping-approach-reveals-the-composite-origin-of-the-connecting-tubule-and-alerts-on-single-cell-specific-ko-model-of-the-distal-nephron
#13
Francesco Trepiccione, Christelle Soukaseum, Anna Iervolino, Federica Petrillo, Miriam Zacchia, Gunther Schütz, Dominique Eladari, Giovambattista Capasso, Juliette Hadchouel
The distal nephron is a heterogeneous part of the nephron composed by six different cell types forming the epithelium of the distal convolute (DCT), connecting (CNT) and collecting duct (CD). To dissect the function of these cells, knock out models specific for their unique cell marker have been created. However, since this part of the nephron develops at the border between the ureteric bud and the metanephric mesenchyme, the specificity of the single cell-markers has been recently questioned. Here, by mapping the fate of the AQP2, NCC-positive cells using transgenic mouse lines expressing the YFP fluorescent marker, we showed that the origin of the distal nephron is extremely composite...
August 31, 2016: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/27582097/functionomics-of-ncc-mutations-in-gitelman-syndrome-using-a-novel-mammalian-cell-based-activity-assay
#14
Marco A Valdez-Flores, Rosa Vargas-Poussou, Sjoerd Verkaart, Omar A Z Tutakhel, Angel Valdez-Ortiz, Anne Blanchard, Cyrielle Treard, Joost G J Hoenderop, René J M Bindels, Sabina Jeleń
Gitelman syndrome (GS) is an autosomal recessive salt-wasting tubular disorder resulting from loss-of-function mutations in the thiazide-sensitive NaCl cotransporter (NCC). Functional analysis of these mutations has been limited to the use of Xenopus laevis oocytes. The aim of the present study was, therefore, to analyze the functional consequences of NCC mutations in a mammalian cell-based assay, followed by analysis of mutated NCC protein expression as well as glycosylation and phosphorylation profiles using human embryonic kidney (HEK) 293 cells...
December 1, 2016: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/27562425/h-k-atpase-type-2-contributes-to-salt-sensitive-hypertension-induced-by-k-restriction
#15
Christine Walter, Mariem Ben Tanfous, Katia Igoudjil, Amel Salhi, Geneviève Escher, Gilles Crambert
In industrialized countries, a large part of the population is daily exposed to low K(+) intake, a situation correlated with the development of salt-sensitive hypertension. Among many processes, adaptation to K(+)-restriction involves the stimulation of H,K-ATPase type 2 (HKA2) in the kidney and colon and, in this study, we have investigated whether HKA2 also contributes to the determination of blood pressure (BP). By using wild-type (WT) and HKA2-null mice (HKA2 KO), we showed that after 4 days of K(+) restriction, WT remain normokalemic and normotensive (112 ± 3 mmHg) whereas HKA2 KO mice exhibit hypokalemia and hypotension (104 ± 2 mmHg)...
October 2016: Pflügers Archiv: European Journal of Physiology
https://www.readbyqxmd.com/read/27508833/-op-7c-01-uromodulin-nacl-interaction-on-mrna-expression-of-ion-transporters-in-isolated-tubules-of-umod-and-umod-mice
#16
L Graham, D Graham, M W McBride, A F Dominiczak, S Padmanabhan
OBJECTIVE: UMOD-/- mice have low blood pressure and decreased salt-sensitivity indicating interactions between UMOD and sodium transport in the TAL. However, it's unclear whether the effect of UMOD is solely through interaction with cognate molecules in the TAL or whether the perturbations in physiology are more complex with involvement of both TAL and other parts of the nephron. We propose to answer this by profiling mRNA expression levels of the main ion transporters and signalling molecules in tubules from UMOD+/+ and UMOD-/- mice...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27508683/-op-lb01-10-the-skipping-of-exon-9-in-cullin-3-causes-a-severe-form-of-familial-hyperkalemic-hypertension-in-mice
#17
C Rafael, W Abdel Khalek, I Kouranti, E Clauser, X Jeunemaitre, J Hadchouel
OBJECTIVE: Familial Hyperkalemic Hypertension (FHHt) is caused by mutations in WNK1, WNK4, KLHL3 or CUL3 (cullin-3). Patients with CUL3 mutation display a more severe phenotype. The mechanisms associated with this severity remain unclear. DESIGN AND METHOD: All CUL3 mutations result in the skipping of exon 9. We have generated a mouse model of "Cul3-FHHt" by deleting Cul3 exon 9. RESULTS: RT-PCR proved that the exon skipping occurred as expected in the kidney of Cul3+/d9 mice...
September 2016: Journal of Hypertension
https://www.readbyqxmd.com/read/27457700/extracellular-k-rapidly-controls-nacl-cotransporter-phosphorylation-in-the-native-distal-convoluted-tubule-by-cl-dependent-and-independent-mechanisms
#18
David Penton, Jan Czogalla, Agnieszka Wengi, Nina Himmerkus, Dominique Loffing-Cueni, Monique Carrel, Renuga Devi Rajaram, Olivier Staub, Markus Bleich, Frank Schweda, Johannes Loffing
KEY POINTS: High dietary potassium (K(+) ) intake dephosphorylates and inactivates the NaCl cotransporter (NCC) in the renal distal convoluted tubule (DCT). Using several ex vivo models, we show that physiological changes in extracellular K(+) , similar to those occurring after a K(+) rich diet, are sufficient to promote a very rapid dephosphorylation of NCC in native DCT cells. Although the increase of NCC phosphorylation upon decreased extracellular K(+) appears to depend on cellular Cl(-) fluxes, the rapid NCC dephosphorylation in response to increased extracellular K(+) is not Cl(-) -dependent...
November 1, 2016: Journal of Physiology
https://www.readbyqxmd.com/read/27443990/renal-sodium-transport-in-renin-deficient-dahl-salt-sensitive-rats
#19
Tengis S Pavlov, Vladislav Levchenko, Daria V Ilatovskaya, Carol Moreno, Alexander Staruschenko
OBJECTIVE: The Dahl salt-sensitive rat is a well-established model of salt-sensitive hypertension. The goal of this study was to assess the expression and activity of renal sodium channels and transporters in the renin-deficient salt-sensitive rat. METHODS: Renin knockout (Ren(-/-)) rats created on the salt-sensitive rat background were used to investigate the role of renin in the regulation of ion transport in salt-sensitive hypertension. Western blotting and patch-clamp analyses were utilized to assess the expression level and activity of Na(+) transporters...
July 2016: Journal of the Renin-angiotensin-aldosterone System: JRAAS
https://www.readbyqxmd.com/read/27442254/prostaglandin-e2-mediated-increase-in-calcium-and-phosphate-excretion-in-a-mouse-model-of-distal-nephron-salt-wasting
#20
Manoocher Soleimani, Sharon Barone, Jie Xu, Saeed Alshahrani, Marybeth Brooks, Francis X McCormack, Roger D Smith, Kamyar Zahedi
Contribution of salt wasting and volume depletion to the pathogenesis of hypercalciuria and hyperphosphaturia is poorly understood. Pendrin/NCC double KO (pendrin/NCC-dKO) mice display severe salt wasting under basal conditions and develop profound volume depletion, prerenal renal failure, and metabolic alkalosis and are growth retarded. Microscopic examination of the kidneys of pendrin/NCC-dKO mice revealed the presence of calcium phosphate deposits in the medullary collecting ducts, along with increased urinary calcium and phosphate excretion...
2016: PloS One
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