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[PMID]:28700713
[Au] Autor:Peng X; Jiang L; Chen C; Qin Y; Yuan T; Wang O; Xing X; Li X; Nie M; Chen L
[Ad] Endereço:Department of Nephrology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
[Ti] Título:Increased urinary prostaglandin E2 metabolite: A potential therapeutic target of Gitelman syndrome.
[So] Source:PLoS One;12(7):e0180811, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Gitelman syndrome (GS), an inherited autosomal recessive salt-losing renal tubulopathy caused by mutations in SLC12A3 gene, has been associated with normal prostaglandin E2 (PGE2) levels since 1995 by a study involving 11 clinically diagnosed patients. However, it is difficult to explain why cyclooxygenase-2 (COX2) inhibitors, which pharmacologically reduce PGE2 synthesis, are helpful to patients with GS, and few studies performed in the last 20 years have measured PGE2 levels. The relationships between the clinical manifestations and PGE2 levels were never thoroughly analyzed. METHODS: This study involved 39 GS patients diagnosed by SLC12A3 gene sequencing. Plasma and 24-h urine samples as well as the clinical data were collected at admission. PGE2 and PGEM levels were detected in plasma and urine samples by enzyme immunoassays. The in vivo function of the sodium-chloride co-transporter (NCC) in GS patients was evaluated using a modified thiazide test. The association among PGE2 levels, clinical manifestations and the function of NCC in GS patients were analyzed. RESULTS: Significantly higher levels of urinary and plasma PGEM were observed in GS patients than in the healthy volunteers. Higher urinary PGEM levels indicated more severe clinical manifestations and NCC dysfunction estimated by the increase of Cl- clearance. A higher PGEM level was found in male GS patients, who showed earlier onset age and more severe hypokalemia, hypochloremia and metabolic alkalosis than female GS patients. No relationship between renin angiotensin aldosterone system activation and PGEM level was observed. CONCLUSIONS: Higher urinary PGEM levels indicated more severe clinical manifestations and NCC dysfunction in GS patients. COX2 inhibition might be a potential therapeutic target in GS patients with elevated PGEM levels.
[Mh] Termos MeSH primário: Dinoprostona/sangue
Dinoprostona/urina
Síndrome de Gitelman/sangue
Síndrome de Gitelman/urina
[Mh] Termos MeSH secundário: Adolescente
Adulto
Ciclo-Oxigenase 2/genética
Ciclo-Oxigenase 2/metabolismo
Inibidores de Ciclo-Oxigenase 2/uso terapêutico
Dinoprostona/metabolismo
Feminino
Síndrome de Gitelman/tratamento farmacológico
Síndrome de Gitelman/genética
Seres Humanos
Modelos Logísticos
Masculino
Mutação/genética
Membro 3 da Família 12 de Carreador de Soluto/genética
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclooxygenase 2 Inhibitors); 0 (Solute Carrier Family 12, Member 3); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (PTGS2 protein, human); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180811


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[PMID]:28566500
[Au] Autor:Li J; Hatano R; Xu S; Wan L; Yang L; Weinstein AM; Palmer L; Wang T
[Ad] Endereço:Department of Cellular and Molecular Physiology, Yale University, New Haven, Connecticut.
[Ti] Título:Gender difference in kidney electrolyte transport. I. Role of AT receptor in thiazide-sensitive Na -Cl cotransporter activity and expression in male and female mice.
[So] Source:Am J Physiol Renal Physiol;313(2):F505-F513, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We studied gender differences in Na -Cl cotransporter (NCC) activity and expression in wild-type (WT) and AT receptor knockout (KO) mice. In renal clearance experiments, urine volume (UV), glomerular filtration rate, absolute Na (E ) and K (E ), and fractional Na (FE ) and K excretion were measured and compared at peak changes after bolus intravenous injection of hydrochlorothiazide (HCTZ; 30 mg/kg). In WT, females responded more strongly than males to HCTZ, with larger fractional increases of UV (7.8- vs. 3.4-fold), E (11.7- vs. 5.7-fold), FE (7.9- vs. 4.9-fold), and E (2.8- vs. 1.4-fold). In contrast, there were no gender differences in the responses to the diuretic in KO mice; HCTZ produced greater effects on male KO than on WT but similar effects on females. In WT, total (tNCC) and phosphorylated (pNCC) NCC protein expressions were 1.8- and 4.6-fold higher in females compared with males ( < 0.05), consistent with the larger response to HCTZ. In KO mice, tNCC and pNCC increased significantly in males to levels not different from those in females. There were no gender differences in the expression of the Na /H exchanger (NHE3) in WT; NHE3 protein decreased to similar extents in male and female KO animals, suggesting AT -mediated NHE3 expression in proximal tubules. The resulting increase in delivery of NaCl to the distal nephron may underlie increased NCC expression and activity in mice lacking the AT receptor.
[Mh] Termos MeSH primário: Angiotensina II/metabolismo
Receptor Tipo 1 de Angiotensina/metabolismo
Caracteres Sexuais
Trocadores de Sódio-Hidrogênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Diurese
Feminino
Hidroclorotiazida
Rim/metabolismo
Masculino
Camundongos Knockout
Natriurese
Fenótipo
Proteínas Serina-Treonina Quinases/metabolismo
Receptor Tipo 1 de Angiotensina/genética
Receptores de Droga/metabolismo
Simportadores de Cloreto de Sódio/metabolismo
Trocador 3 de Sódio-Hidrogênio
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptor, Angiotensin, Type 1); 0 (Receptors, Drug); 0 (Slc12a3 protein, mouse); 0 (Slc9a3 protein, mouse); 0 (Sodium Chloride Symporters); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); 0 (Solute Carrier Family 12, Member 3); 0 (thiazide receptor); 0J48LPH2TH (Hydrochlorothiazide); 11128-99-7 (Angiotensin II); EC 2.7.1.- (Prkwnk4 protein, mouse); EC 2.7.1.- (Stk39 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00087.2017


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[PMID]:28515174
[Au] Autor:Rosenbaek LL; Rizzo F; MacAulay N; Staub O; Fenton RA
[Ad] Endereço:InterPrET Center, Department of Biomedicine, Aarhus University, Aarhus, Denmark.
[Ti] Título:Functional assessment of sodium chloride cotransporter NCC mutants in polarized mammalian epithelial cells.
[So] Source:Am J Physiol Renal Physiol;313(2):F495-F504, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The thiazide-sensitive sodium chloride cotransporter NCC is important for maintaining serum sodium (Na ) and, indirectly, serum potassium (K ) levels. Functional studies on NCC have used cell lines with native NCC expression, transiently transfected nonpolarized cell lines, or oocytes. Here, we developed the use of polarized Madin-Darby canine kidney type I (MDCKI) mammalian epithelial cell lines with tetracycline-inducible human NCC expression to study NCC activity and membrane abundance in the same system. In radiotracer assays, induced cells grown on filters had robust thiazide-sensitive and chloride dependent sodium-22 ( Na) uptake from the apical side. To minimize cost and maximize throughput, assays were modified to use cells grown on plastic. On plastic, cells had similar thiazide-sensitive Na uptakes that increased following preincubation of cells in chloride-free solutions. NCC was detected in the plasma membrane, and both membrane abundance and phosphorylation of NCC were increased by incubation in chloride-free solutions. Furthermore, in cells exposed for 15 min to low or high extracellular K , the levels of phosphorylated NCC increased and decreased, respectively. To demonstrate that the system allows rapid and systematic assessment of mutated NCC, three phosphorylation sites in NCC were mutated, and NCC activity was examined. Na fluxes in phosphorylation-deficient mutants were reduced to baseline levels, whereas phosphorylation-mimicking mutants were constitutively active, even without chloride-free stimulation. In conclusion, this system allows the activity, cellular localization, and abundance of wild-type or mutant NCC to be examined in the same polarized mammalian expression system in a rapid, easy, and low-cost fashion.
[Mh] Termos MeSH primário: Polaridade Celular
Cloretos/metabolismo
Células Epiteliais/metabolismo
Mutação
Sódio/metabolismo
[Mh] Termos MeSH secundário: Animais
Técnicas de Cultura de Células
Cães
Relação Dose-Resposta a Droga
Células Epiteliais/efeitos dos fármacos
Genótipo
Ensaios de Triagem em Larga Escala
Cinética
Células Madin Darby de Rim Canino
Fenótipo
Fosforilação
Potássio/metabolismo
Processamento de Proteína Pós-Traducional
Inibidores de Simportadores de Cloreto de Sódio/farmacologia
Membro 3 da Família 12 de Carreador de Soluto/efeitos dos fármacos
Membro 3 da Família 12 de Carreador de Soluto/genética
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
Transfecção
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chlorides); 0 (SLC12A3 protein, human); 0 (Sodium Chloride Symporter Inhibitors); 0 (Solute Carrier Family 12, Member 3); 9NEZ333N27 (Sodium); RWP5GA015D (Potassium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00088.2017


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[PMID]:28515172
[Au] Autor:Wang L; Song J; Wang S; Buggs J; Chen R; Zhang J; Wang L; Rong S; Li W; Wei J; Liu R
[Ad] Endereço:Department of Molecular Pharmacology and Physiology, University of South Florida College of Medicine, Tampa, Florida; leiwang@health.usf.edu.
[Ti] Título:Cross-sex transplantation alters gene expression and enhances inflammatory response in the transplanted kidneys.
[So] Source:Am J Physiol Renal Physiol;313(2):F326-F338, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kidney transplantation (KTX) is a life-saving procedure for patients with end-stage renal disease. Expression levels of many genes in the kidney vary between males and females, which may play an essential role in the sex differences in graft function. However, whether these differences are affected after cross-sex-KTX is unknown. In the present study, we assessed postoperative changes in genotype, function, and inflammatory responses of the grafts in same-sex- and cross-sex-KTX. Single kidney transplants were performed between same and different sex C57BL/6 mice paired into four combination groups: female donor/female recipient (F/F); male donor/male recipient (M/M); female donor/male recipient (F/M); and male donor/female recipient (M/F). The remnant native kidney was removed 4 days posttransplant. Expression levels of genes related to the contractility of the afferent arteriole and tubular sodium reabsorption were assessed. Same-sex-KTX did not significantly alter the magnitude or sex difference pattern of gene expression in male or female grafts. Cross-sex-KTX showed an attenuated sex difference in gene expressions. The measurements of endothelin 1, endothelin ET receptor, Na -K -2Cl cotransporter 2 (NKCC2), and epithelial Na channels (ENaC) subunits exhibited decreases in M/F compared with M/M and increases in F/M compared with F/F. There were no significant differences in hemodynamics or sodium excretion in response to acute volume expansion for any sex combinations. Cross-sex-KTX stimulated more robust inflammatory responses than same-sex-KTX. IL-6 and KC mRNA levels elevated 5- to 20-fold in cross-sex-KTX compared with same-sex-KTX. In conclusion, cross-sex-KTX alters gene expression levels and induces inflammatory responses, which might play an important role in long-term graft function.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Transplante de Rim/efeitos adversos
Rim/metabolismo
Rim/cirurgia
Nefrite/genética
[Mh] Termos MeSH secundário: Animais
Endotelina-1/genética
Endotelina-1/metabolismo
Canais Epiteliais de Sódio/genética
Canais Epiteliais de Sódio/metabolismo
Feminino
Interação Gene-Ambiente
Genótipo
Hemodinâmica
Mediadores da Inflamação/metabolismo
Rim/irrigação sanguínea
Rim/patologia
Masculino
Camundongos Endogâmicos C57BL
Modelos Animais
Nefrite/metabolismo
Nefrite/patologia
Nefrite/fisiopatologia
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Receptores de Angiotensina/genética
Receptores de Angiotensina/metabolismo
Receptores de Endotelina/genética
Receptores de Endotelina/metabolismo
Circulação Renal
Eliminação Renal
Fatores Sexuais
Sódio/metabolismo
Trocador 3 de Sódio-Hidrogênio
Trocadores de Sódio-Hidrogênio/genética
Trocadores de Sódio-Hidrogênio/metabolismo
Membro 1 da Família 12 de Carreador de Soluto/genética
Membro 1 da Família 12 de Carreador de Soluto/metabolismo
Membro 3 da Família 12 de Carreador de Soluto/genética
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin-1); 0 (Epithelial Sodium Channels); 0 (Inflammation Mediators); 0 (RNA, Messenger); 0 (Receptors, Angiotensin); 0 (Receptors, Endothelin); 0 (Slc12a1 protein, mouse); 0 (Slc12a3 protein, mouse); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); 0 (Solute Carrier Family 12, Member 1); 0 (Solute Carrier Family 12, Member 3); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170519
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00039.2017


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[PMID]:28442491
[Au] Autor:Grimm PR; Coleman R; Delpire E; Welling PA
[Ad] Endereço:Department of Physiology, Maryland Kidney Discovery Center, University of Maryland Medical School, Baltimore, Maryland; and.
[Ti] Título:Constitutively Active SPAK Causes Hyperkalemia by Activating NCC and Remodeling Distal Tubules.
[So] Source:J Am Soc Nephrol;28(9):2597-2606, 2017 Sep.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo: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 gene, which encodes the terminal kinase in the WNK signaling pathway, Ste20-related proline-alanine-rich kinase (SPAK). Renal expression of the constitutively active (CA)-SPAK mutant was specifically targeted to the early DCT using a DCT-driven Cre recombinase. CA-SPAK mice displayed thiazide-treatable hypertension and hyperkalemia, concurrent with NCC hyperphosphorylation. However, thiazide-mediated inhibition of NCC and consequent restoration of sodium excretion did not immediately restore urinary potassium excretion in CA-SPAK mice. Notably, CA-SPAK mice exhibited ASDN remodeling, involving a reduction in connecting tubule mass and attenuation of epithelial sodium channel (ENaC) and ROMK expression and apical localization. Blocking hyperactive NCC in the DCT gradually restored ASDN structure and ENaC and ROMK expression, concurrent with the restoration of urinary potassium excretion. These findings verify that NCC hyperactivity underlies FHHt but also reveal that NCC-dependent changes in the driving force for potassium secretion are not sufficient to explain hyperkalemia. Instead, a DCT-ASDN coupling process controls potassium balance in health and becomes aberrantly activated in FHHt.
[Mh] Termos MeSH primário: Hidroclorotiazida/farmacologia
Túbulos Renais Distais/patologia
Proteínas Serina-Treonina Quinases/metabolismo
Pseudo-Hipoaldosteronismo/metabolismo
Inibidores de Simportadores de Cloreto de Sódio/farmacologia
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
[Mh] Termos MeSH secundário: Aldosterona/metabolismo
Animais
Pressão Sanguínea/efeitos dos fármacos
Canais Epiteliais de Sódio/metabolismo
Hidroclorotiazida/uso terapêutico
Túbulos Renais Distais/metabolismo
Camundongos
Natriurese/efeitos dos fármacos
Fosforilação
Potássio/urina
Canais de Potássio Corretores do Fluxo de Internalização/metabolismo
Proteínas Serina-Treonina Quinases/genética
Pseudo-Hipoaldosteronismo/tratamento farmacológico
Pseudo-Hipoaldosteronismo/genética
Pseudo-Hipoaldosteronismo/urina
Transdução de Sinais
Inibidores de Simportadores de Cloreto de Sódio/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epithelial Sodium Channels); 0 (Kcnj1 protein, mouse); 0 (Potassium Channels, Inwardly Rectifying); 0 (Sodium Chloride Symporter Inhibitors); 0 (Solute Carrier Family 12, Member 3); 0J48LPH2TH (Hydrochlorothiazide); 4964P6T9RB (Aldosterone); EC 2.7.1.- (Stk39 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); RWP5GA015D (Potassium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016090948


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[PMID]:28356292
[Au] Autor:Frindt G; Yang L; Uchida S; Weinstein AM; Palmer LG
[Ad] Endereço:Department of Physiology and Biophysics, Weill-Cornell Medical College, New York, New York.
[Ti] Título:Responses of distal nephron Na transporters to acute volume depletion and hyperkalemia.
[So] Source:Am J Physiol Renal Physiol;313(1):F62-F73, 2017 Jul 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We assessed effects of acute volume reductions induced by administration of diuretics in rats. Direct block of Na transport produced changes in urinary electrolyte excretion. Adaptations to these effects appeared as alterations in the expression of protein for the distal nephron Na transporters NCC and ENaC. Two hours after a single injection of furosemide (6 mg/kg) or hydrochlorothiazide (HCTZ; 30 mg/kg) Na and K excretion increased but no changes in the content of activated forms of NCC (phosphorylated on residue T53) or ENaC (cleaved γ-subunit) were detected. In contrast, amiloride (0.6 mg/kg) evoked a similar natriuresis that coincided with decreased pT53NCC and increased cleaved γENaC. Alterations in posttranslational membrane protein processing correlated with an increase in plasma K of 0.6-0.8 mM. Decreased pT53NCC occurred within 1 h after amiloride injection, whereas changes in γENaC were slower and were blocked by the mineralocorticoid receptor antagonist spironolactone. Increased γENaC cleavage correlated with elevation of the surface expression of the subunit as assessed by in situ biotinylation. Na depletion induced by 2 h of furosemide or HCTZ treatment increases total NCC expression without affecting ENaC protein. However, restriction of Na intake for 10 h (during the day) or 18 h (overnight) increased the abundance of both total NCC and of cleaved α- and γENaC. We conclude that the kidneys respond acutely to hyperkalemic challenges by decreasing the activity of NCC while increasing that of ENaC. They respond to hypovolemia more slowly, increasing Na reabsorptive capacities of both of these transporters.
[Mh] Termos MeSH primário: Diuréticos/farmacologia
Canais Epiteliais de Sódio/efeitos dos fármacos
Hiperpotassemia/metabolismo
Hipovolemia/metabolismo
Néfrons/efeitos dos fármacos
Potássio/metabolismo
Sódio/metabolismo
[Mh] Termos MeSH secundário: Amilorida/farmacologia
Animais
Diuréticos/toxicidade
Canais Epiteliais de Sódio/metabolismo
Feminino
Furosemida/farmacologia
Hidroclorotiazida/farmacologia
Hiperpotassemia/sangue
Hiperpotassemia/induzido quimicamente
Hiperpotassemia/urina
Hipovolemia/sangue
Hipovolemia/induzido quimicamente
Hipovolemia/urina
Masculino
Modelos Biológicos
Néfrons/metabolismo
Fosforilação
Potássio/sangue
Potássio/urina
Ratos Sprague-Dawley
Eliminação Renal/efeitos dos fármacos
Sódio/sangue
Sódio/urina
Membro 3 da Família 12 de Carreador de Soluto/efeitos dos fármacos
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
Espironolactona/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diuretics); 0 (Epithelial Sodium Channels); 0 (Scnn1g protein, rat); 0 (Slc12a3 protein, rat); 0 (Solute Carrier Family 12, Member 3); 0J48LPH2TH (Hydrochlorothiazide); 27O7W4T232 (Spironolactone); 7DZO8EB0Z3 (Amiloride); 7LXU5N7ZO5 (Furosemide); 9NEZ333N27 (Sodium); RWP5GA015D (Potassium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00668.2016


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[PMID]:28341239
[Au] Autor:Shoda W; Nomura N; Ando F; Mori Y; Mori T; Sohara E; Rai T; Uchida S
[Ad] Endereço:Department of Nephrology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan.
[Ti] Título:Calcineurin inhibitors block sodium-chloride cotransporter dephosphorylation in response to high potassium intake.
[So] Source:Kidney Int;91(2):402-411, 2017 Feb.
[Is] ISSN:1523-1755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dietary potassium intake is inversely related to blood pressure and mortality. Moreover, the sodium-chloride cotransporter (NCC) plays an important role in blood pressure regulation and urinary potassium excretion in response to potassium intake. Previously, it was shown that NCC is activated by the WNK4-SPAK cascade and dephosphorylated by protein phosphatase. However, the mechanism of NCC regulation with acute potassium intake is still unclear. To identify the molecular mechanism of NCC regulation in response to potassium intake, we used adult C57BL/6 mice fed a 1.7% potassium solution by oral gavage. We confirmed that acute potassium load rapidly dephosphorylated NCC, which was not dependent on the accompanying anions. Mice were treated with tacrolimus (calcineurin inhibitor) and W7 (calmodulin inhibitor) before the oral potassium loads. Dephosphorylation of NCC induced by potassium was significantly inhibited by both tacrolimus and W7 treatment. There was no significant difference in WNK4, OSR1, and SPAK expression after high potassium intake, even after tacrolimus and W7 treatment. Another phosphatase, protein phosphatase 1, and its endogenous inhibitor I-1 did not show a significant change after potassium intake. Hyperkaliuria, induced by high potassium intake, was significantly suppressed by tacrolimus treatment. Thus, calcineurin is activated by an acute potassium load, which rapidly dephosphorylates NCC, leading to increased urinary potassium excretion.
[Mh] Termos MeSH primário: Inibidores de Calcineurina/farmacologia
Calcineurina/metabolismo
Rim/efeitos dos fármacos
Potássio na Dieta/metabolismo
Eliminação Renal/efeitos dos fármacos
Tacrolimo/farmacologia
[Mh] Termos MeSH secundário: Animais
Proteínas Quinases Dependentes de Cálcio-Calmodulina/antagonistas & inibidores
Proteínas Quinases Dependentes de Cálcio-Calmodulina/metabolismo
Concentração de Íons de Hidrogênio
Rim/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Fosforilação
Potássio na Dieta/sangue
Potássio na Dieta/urina
Inibidores de Proteínas Quinases/farmacologia
Proteína Fosfatase 1/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Transdução de Sinais/efeitos dos fármacos
Membro 3 da Família 12 de Carreador de Soluto/efeitos dos fármacos
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
Sulfonamidas/farmacologia
Fatores de Tempo
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcineurin Inhibitors); 0 (Osr1 protein, mouse); 0 (Potassium, Dietary); 0 (Protein Kinase Inhibitors); 0 (Slc12a3 protein, mouse); 0 (Solute Carrier Family 12, Member 3); 0 (Sulfonamides); 0 (Transcription Factors); 65595-90-6 (W 7); EC 2.7.1.- (Prkwnk4 protein, mouse); EC 2.7.1.- (Stk39 protein, mouse); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases); EC 3.1.3.16 (Calcineurin); EC 3.1.3.16 (Protein Phosphatase 1); WM0HAQ4WNM (Tacrolimus)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170326
[St] Status:MEDLINE


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[PMID]:28331059
[Au] Autor:Layton AT; Edwards A; Vallon V
[Ad] Endereço:Department of Mathematics, Duke University, Durham, North Carolina; alayton@math.duke.edu.
[Ti] Título:Adaptive changes in GFR, tubular morphology, and transport in subtotal nephrectomized kidneys: modeling and analysis.
[So] Source:Am J Physiol Renal Physiol;313(2):F199-F209, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Removal of renal mass stimulates anatomical and functional adaptations in the surviving nephrons, including elevations in single-nephron glomerular filtration rate (SNGFR) and tubular hypertrophy. A goal of this study is to assess the extent to which the concomitant increases in filtered load and tubular transport capacity preserve homeostasis of water and salt. To accomplish that goal, we developed computational models to simulate solute transport and metabolism along nephron populations in a uninephrectomized (UNX) rat and a 5/6-nephrectomized (5/6-NX) rat. Model simulations indicate that nephrectomy-induced SNGFR increase and tubular hypertrophy go a long way to normalize excretion, but alone are insufficient to fully maintain salt balance. We then identified increases in the protein density of Na -K -ATPase, Na -K -2Cl cotransporter, Na -Cl cotransporter, and epithelial Na channel, such that the UNX and 5/6-NX models predict urine flow and urinary Na and K excretions that are similar to sham levels. The models predict that, in the UNX and 5/6-NX kidneys, fractional water and salt reabsorption is similar to sham along the initial nephron segments (i.e., from the proximal tubule to the distal convoluted tubule), with a need to further reduce Na reabsorption and increase K secretion primarily along the connecting tubules and collecting ducts to achieve balance. Additionally, the models predict that, given the substantially elevated filtered and thus transport load among each of the surviving nephrons, oxygen consumption per nephron segment in a UNX or 5/6-NX kidney increases substantially. But due to the reduced nephron population, whole animal renal oxygen consumption is lower. The efficiency of tubular Na transport in the UNX and 5/6-NX kidneys is predicted to be similar to sham.
[Mh] Termos MeSH primário: Células Epiteliais/metabolismo
Taxa de Filtração Glomerular
Túbulos Renais/metabolismo
Túbulos Renais/cirurgia
Modelos Biológicos
Nefrectomia/métodos
[Mh] Termos MeSH secundário: Adaptação Fisiológica
Animais
Células Epiteliais/patologia
Canais Epiteliais de Sódio/metabolismo
Túbulos Renais/patologia
Túbulos Renais/fisiopatologia
Modelos Animais
Nefrectomia/efeitos adversos
Potássio/metabolismo
Ratos
Eliminação Renal
Reabsorção Renal
Sódio/metabolismo
Simportadores de Cloreto de Sódio-Potássio/metabolismo
ATPase Trocadora de Sódio-Potássio/metabolismo
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epithelial Sodium Channels); 0 (Slc12a3 protein, rat); 0 (Sodium-Potassium-Chloride Symporters); 0 (Solute Carrier Family 12, Member 3); 9NEZ333N27 (Sodium); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); RWP5GA015D (Potassium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00018.2017


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[PMID]:28274929
[Au] Autor:Pathare G; Tutakhel OAZ; van der Wel MC; Shelton LM; Deinum J; Lenders JWM; Hoenderop JGJ; Bindels RJM
[Ad] Endereço:Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands.
[Ti] Título:Hydrochlorothiazide treatment increases the abundance of the NaCl cotransporter in urinary extracellular vesicles of essential hypertensive patients.
[So] Source:Am J Physiol Renal Physiol;312(6):F1063-F1072, 2017 Jun 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The thiazide-sensitive NaCl cotransporter (NCC), located apically in distal convoluted tubule epithelia, regulates the fine-tuning of renal sodium excretion. Three isoforms of NCC are generated through alternative splicing of the transcript, of which the third isoform has been the most extensively investigated in pathophysiological conditions. The aim of this study was to investigate the effect of different anti-hypertensive treatments on the abundance and phosphorylation of all three NCC isoforms in urinary extracellular vesicles (uEVs) of essential hypertensive patients. In uEVs isolated from patients ( = 23) before and after hydrochlorothiazide or valsartan treatment, the abundance and phosphorylation of the NCC isoforms was determined. Additionally, clinical biochemistry and blood pressure of the patients was assessed. Our results show that NCC detected in human uEVs has a glycosylated and oligomeric structure, comparable to NCC present in human kidney membrane fractions. Despite the inhibitory action of hydrochlorothiazide on NCC activity, immunoblot analysis of uEVs showed significantly increased abundance of NCC isoforms 1 and 2 (NCC ), total NCC (NCC ), and the phosphorylated form of total NCC (pNCC -T55/T60) in essential hypertensive patients treated with hydrochlorothiazide but not with valsartan. This study highlights that NCC , NCC , and pNCC -T55/T60 are upregulated by hydrochlorothiazide, and the increase in NCC abundance in uEVs of essential hypertensive patients correlates with the blood pressure response to hydrochlorothiazide.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/uso terapêutico
Anti-Hipertensivos/uso terapêutico
Vesículas Extracelulares/efeitos dos fármacos
Hidroclorotiazida/uso terapêutico
Hipertensão/tratamento farmacológico
Rim/efeitos dos fármacos
Inibidores de Simportadores de Cloreto de Sódio/uso terapêutico
Valsartana/uso terapêutico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Biomarcadores/urina
Pressão Sanguínea/efeitos dos fármacos
Estudos Cross-Over
Vesículas Extracelulares/metabolismo
Feminino
Glicosilação
Seres Humanos
Hipertensão/fisiopatologia
Hipertensão/urina
Rim/metabolismo
Rim/fisiopatologia
Masculino
Meia-Idade
Países Baixos
Fosforilação
Estudos Prospectivos
Isoformas de Proteínas
Membro 3 da Família 12 de Carreador de Soluto/efeitos dos fármacos
Membro 3 da Família 12 de Carreador de Soluto/urina
Resultado do Tratamento
Regulação para Cima
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL; COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Antihypertensive Agents); 0 (Biomarkers); 0 (Protein Isoforms); 0 (SLC12A3 protein, human); 0 (Sodium Chloride Symporter Inhibitors); 0 (Solute Carrier Family 12, Member 3); 0J48LPH2TH (Hydrochlorothiazide); 80M03YXJ7I (Valsartan)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00644.2016


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[PMID]:28274925
[Au] Autor:Slattery P; Frölich S; Goren I; Nüsing RM
[Ad] Endereço:Institute of Clinical Pharmacology, Goethe-University, Frankfurt, Germany; and.
[Ti] Título:Salt supplementation ameliorates developmental kidney defects in COX-2 mice.
[So] Source:Am J Physiol Renal Physiol;312(6):F1044-F1055, 2017 Jun 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Deficiency of cyclooxygenase-2 (COX-2) activity in the early postnatal period causes impairment of kidney development leading to kidney insufficiency. We hypothesize that impaired NaCl reabsorption during the first days of life is a substantial cause for nephrogenic defects observed in COX-2 mice and that salt supplementation corrects these defects. Daily injections of NaCl (0.8 mg·g ·day ) for the first 10 days after birth ameliorated impaired kidney development in COX-2 pups resulting in an increase in glomerular size and fewer immature superficial glomeruli. However, impaired renal subcortical growth was not corrected. Increasing renal tubular flow by volume load or injections of KCl did not relieve the renal histomorphological damage. Administration of torsemide and spironolactone also affected nephrogenesis resulting in diminished glomeruli and cortical thinning. Treatment of COX-2 pups with NaCl/DOCA caused a stronger mitigation of glomerular size and induced a slight but significant growth of cortical tissue mass. After birth, renal mRNA expression of NHE3, NKCC2, ROMK, NCCT, ENaC, and Na /K -ATPase increased relative to postnatal day 2 in wild-type mice. However, in COX-2 mice, a significantly lower expression was observed for NCCT, whereas NaCl/DOCA treatment significantly increased NHE3 and ROMK expression. Long-term effects of postnatal NaCl/DOCA injections indicate improved kidney function with normalization of pathologically enhanced creatinine and urea plasma levels; also, albumin excretion was observed. In summary, we present evidence that salt supplementation during the COX-2-dependent time frame of nephrogenesis partly reverses renal morphological defects in COX-2 mice and improves kidney function.
[Mh] Termos MeSH primário: Ciclo-Oxigenase 2/deficiência
Rim/efeitos dos fármacos
Cloreto de Sódio na Dieta/administração & dosagem
Anormalidades Urogenitais/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Ciclo-Oxigenase 2/genética
Acetato de Desoxicorticosterona/administração & dosagem
Modelos Animais de Doenças
Canais Epiteliais de Sódio/genética
Canais Epiteliais de Sódio/metabolismo
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Predisposição Genética para Doença
Rim/anormalidades
Rim/enzimologia
Rim/crescimento & desenvolvimento
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Antagonistas de Receptores de Mineralocorticoides/farmacologia
Morfogênese
Fenótipo
Canais de Potássio Corretores do Fluxo de Internalização/genética
Canais de Potássio Corretores do Fluxo de Internalização/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Inibidores de Simportadores de Cloreto de Sódio e Potássio/administração & dosagem
Trocador 3 de Sódio-Hidrogênio
Trocadores de Sódio-Hidrogênio/genética
Trocadores de Sódio-Hidrogênio/metabolismo
ATPase Trocadora de Sódio-Potássio/genética
ATPase Trocadora de Sódio-Potássio/metabolismo
Membro 1 da Família 12 de Carreador de Soluto/genética
Membro 1 da Família 12 de Carreador de Soluto/metabolismo
Membro 3 da Família 12 de Carreador de Soluto/genética
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
Espironolactona/administração & dosagem
Sulfonamidas/administração & dosagem
Anormalidades Urogenitais/enzimologia
Anormalidades Urogenitais/genética
Anormalidades Urogenitais/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epithelial Sodium Channels); 0 (Kcnj1 protein, mouse); 0 (Mineralocorticoid Receptor Antagonists); 0 (Potassium Channels, Inwardly Rectifying); 0 (RNA, Messenger); 0 (Slc12a1 protein, mouse); 0 (Slc12a3 protein, mouse); 0 (Slc9a3 protein, mouse); 0 (Sodium Chloride, Dietary); 0 (Sodium Potassium Chloride Symporter Inhibitors); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); 0 (Solute Carrier Family 12, Member 1); 0 (Solute Carrier Family 12, Member 3); 0 (Sulfonamides); 27O7W4T232 (Spironolactone); 6E0A168OB8 (Desoxycorticosterone Acetate); EC 1.14.99.- (Ptgs2 protein, mouse); EC 1.14.99.1 (Cyclooxygenase 2); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); W31X2H97FB (torsemide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00565.2016



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