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Pesquisa : D12.776.157.530.450.625.750.500 [Categoria DeCS]
Referências encontradas : 379 [refinar]
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[PMID]:28678861
[Au] Autor:de Bragança AC; Moreau RLM; de Brito T; Shimizu MHM; Canale D; de Jesus DA; Silva AMG; Gois PH; Seguro AC; Magaldi AJ
[Ad] Endereço:Clinical Hospital, School of Medicine-Department of Nephrology- Basic Research Laboratory-LIM12, University of Sâo Paulo, SP, Brazil.
[Ti] Título:Ecstasy induces reactive oxygen species, kidney water absorption and rhabdomyolysis in normal rats. Effect of N-acetylcysteine and Allopurinol in oxidative stress and muscle fiber damage.
[So] Source:PLoS One;12(7):e0179199, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ecstasy (Ec) use produces hyperthermia, excessive sweating, intense thirst, an inappropriate antidiuretic hormone secretion (SIADH) and a multisystemic toxicity due to oxidative stress (OS). Intense thirst induces high intake of pure water, which associated with SIADH, usually develops into acute hyponatremia (Hn). As Hn is induced rapidly, experiments to check if Ec acted directly on the Inner Medullary Collecting Ducts (IMCD) of rats were conducted. Rhabdomyolysis and OS were also studied because Ec is known to induce Reactive Oxygen Species (ROS) and tissue damage. To decrease OS, the antioxidant inhibitors N-acetylcysteine (NAC) and Allopurinol (Allo) were used. METHODS: Rats were maintained on a lithium (Li) diet to block the Vasopressin action before Ec innoculation. AQP2 (Aquaporin 2), ENaC (Epitheliun Sodium Channel) and NKCC2 (Sodium, Potassium, 2 Chloride) expression were determined by Western Blot in isolated IMCDs. The TBARS (thiobarbituric acid reactive substances) and GSH (reduced form of Glutathione) were determined in the Ec group (6 rats injected with Ec-10mg/kg), in Ec+NAC groups (NAC 100mg/Kg/bw i.p.) and in Allo+Ec groups (Allo 50mg/Kg/i.p.). RESULTS: Enhanced AQP2 expression revealed that Ec increased water transporter expression, decreased by Li diet, but the expression of the tubular transporters did not change. The Ec, Ec+NAC and Allo+Ec results showed that Ec increased TBARS and decreased GSH, showing evidence of ROS occurrence, which was protected by NAC and Allo. Rhabdomyolysis was only protected by Allo. CONCLUSION: Results showed that Ec induced an increase in AQP2 expression, evidencing another mechanism that might contribute to cause rapid hyponatremia. In addition, they showed that NAC and Allo protected against OS, but only Allo decreased rhabdomyolysis and hyperthermia.
[Mh] Termos MeSH primário: Depuradores de Radicais Livres/farmacologia
Rim/efeitos dos fármacos
Fibras Musculares Esqueléticas/efeitos dos fármacos
N-Metil-3,4-Metilenodioxianfetamina/toxicidade
Estresse Oxidativo/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
Rabdomiólise/induzido quimicamente
[Mh] Termos MeSH secundário: Acetilcisteína/farmacologia
Alopurinol/farmacologia
Animais
Aquaporina 2/metabolismo
Western Blotting
Canais Epiteliais de Sódio/metabolismo
Glutationa/metabolismo
Alucinógenos/toxicidade
Rim/metabolismo
Túbulos Renais Coletores/efeitos dos fármacos
Túbulos Renais Coletores/metabolismo
Masculino
Fibras Musculares Esqueléticas/metabolismo
Fibras Musculares Esqueléticas/patologia
Ratos Wistar
Rabdomiólise/prevenção & controle
Membro 1 da Família 12 de Carreador de Soluto/metabolismo
Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
Água/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aquaporin 2); 0 (Epithelial Sodium Channels); 0 (Free Radical Scavengers); 0 (Hallucinogens); 0 (Reactive Oxygen Species); 0 (Solute Carrier Family 12, Member 1); 0 (Thiobarbituric Acid Reactive Substances); 059QF0KO0R (Water); 63CZ7GJN5I (Allopurinol); GAN16C9B8O (Glutathione); KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine); WYQ7N0BPYC (Acetylcysteine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170706
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179199


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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]: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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[PMID]:28237360
[Au] Autor:Yu G; Cheng M; Wang W; Zhao R; Liu Z
[Ad] Endereço:Zhejiang Provincial Key Laboratory of Medical Genetics, School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, Zhejiang 325003, China.
[Ti] Título:Involvement of WNK1-mediated potassium channels in the sexual dimorphism of blood pressure.
[So] Source:Biochem Biophys Res Commun;485(2):255-260, 2017 Apr 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Potassium homeostasis plays an essential role in the control of blood pressure. It is unknown, however, whether potassium balance is involved in the gender-associated blood pressure differences. We therefore investigated the possible mechanism of sexual dimorphism in blood pressure regulation by measuring the blood pressure, plasma potassium, renal actions of potassium channels and upstream regulator in male and female mice. Here we found that female mice exhibited lower blood pressure and higher plasma K level as compared to male littermates. Western blot analyses of mouse kidney extract revealed a significant decrease in renal outer medullary potassium (ROMK) channel expression, while large-conductance Ca -activated K (BK) channel and Na-K-2Cl cotransporter (NKCC2) as well as the upstream regulator with-no-lysine kinase 1 (WNK1) enhanced in female mice under normal condition. Surprisingly, both dietary K loading and K depletion eliminated the differences in plasma K and blood pressure between females and males, and the differences of renal K channels and WNK1 also attenuated in both groups of mice. These findings indicated the existence of a close correlation between K homeostasis and sex-associated blood pressure. Moreover, the differential regulation of ROMK, BK-α and NKCC2 between female and male mice, at least, were partly mediated via WNK1 pathway, which may contribute to the sexual dimorphism of plasma K and blood pressure control.
[Mh] Termos MeSH primário: Pressão Sanguínea
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/metabolismo
Antígenos de Histocompatibilidade Menor/metabolismo
Canais de Potássio Corretores do Fluxo de Internalização/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Caracteres Sexuais
Membro 1 da Família 12 de Carreador de Soluto/metabolismo
[Mh] Termos MeSH secundário: Animais
Feminino
Rim/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Potássio/sangue
Potássio/metabolismo
Proteína Quinase 1 Deficiente de Lisina WNK
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Kcnj1 protein, mouse); 0 (Kcnma1 protein, mouse); 0 (Large-Conductance Calcium-Activated Potassium Channel alpha Subunits); 0 (Minor Histocompatibility Antigens); 0 (Potassium Channels, Inwardly Rectifying); 0 (Slc12a1 protein, mouse); 0 (Solute Carrier Family 12, Member 1); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (WNK Lysine-Deficient Protein Kinase 1); EC 2.7.11.1 (Wnk1 protein, mouse); RWP5GA015D (Potassium)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170227
[St] Status:MEDLINE


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[PMID]:28228405
[Au] Autor:Araujo M; Welch WJ; Zhou X; Sullivan K; Walsh S; Pasternak A; Wilcox CS
[Ad] Endereço:Hypertension Research Center and Division of Nephrology and Hypertension, Georgetown University, Washington, District of Columbia; and araujo.magali@gmail.com.
[Ti] Título:Inhibition of ROMK blocks macula densa tubuloglomerular feedback yet causes renal vasoconstriction in anesthetized rats.
[So] Source:Am J Physiol Renal Physiol;312(6):F1120-F1127, 2017 Jun 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Na -K -2Cl cotransporter (NKCC2) on the loop of Henle is the site of action of furosemide. Because outer medullary potassium channel (ROMK) inhibitors prevent reabsorption by NKCC2, we tested the hypothesis that ROMK inhibition with a novel selective ROMK inhibitor (compound C) blocks tubuloglomerular feedback (TGF) and reduces vascular resistance. Loop perfusion of either ROMK inhibitor or furosemide caused dose-dependent blunting of TGF, but the response to furosemide was 10-fold more sensitive (IC = 10 M for furosemide and IC = 10 M for compound C). During systemic infusion, both diuretics inhibited TGF, but ROMK inhibitor was 10-fold more sensitive (compound C: 63% inhibition; furosemide: 32% inhibition). Despite blockade of TGF, 1 h of constant systemic infusion of both diuretics reduced the glomerular filtration rate (GFR) and renal blood flow (RBF) by 40-60% and increased renal vascular resistance (RVR) by 100-200%. Neither diuretic altered blood pressure or hematocrit. Proximal tubule hydrostatic pressures (P ) increased transiently with both diuretics (compound C: 56% increase; furosemide: 70% increase) but returned to baseline. ROMK inhibitor caused more natriuresis (3,400 vs. 1,600% increase) and calciuresis (1,200 vs. 800% increase) but less kaliuresis (33 vs. 167% increase) than furosemide. In conclusion, blockade of ROMK or Na -K -2Cl transport inhibits TGF yet increases renal vascular resistance. The renal vasoconstriction was independent of volume depletion, blood pressure, TGF, or P .
[Mh] Termos MeSH primário: Diuréticos/farmacologia
Glomérulos Renais/irrigação sanguínea
Glomérulos Renais/efeitos dos fármacos
Túbulos Renais/irrigação sanguínea
Túbulos Renais/efeitos dos fármacos
Bloqueadores dos Canais de Potássio/farmacologia
Canais de Potássio Corretores do Fluxo de Internalização/antagonistas & inibidores
Vasoconstrição/efeitos dos fármacos
Vasoconstritores/farmacologia
[Mh] Termos MeSH secundário: Anestesia Geral
Animais
Cálcio/urina
Relação Dose-Resposta a Droga
Retroalimentação
Furosemida/farmacologia
Taxa de Filtração Glomerular/efeitos dos fármacos
Pressão Hidrostática
Glomérulos Renais/metabolismo
Túbulos Renais/metabolismo
Masculino
Modelos Animais
Natriurese/efeitos dos fármacos
Potássio/urina
Canais de Potássio Corretores do Fluxo de Internalização/metabolismo
Ratos Sprague-Dawley
Circulação Renal/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Inibidores de Simportadores de Cloreto de Sódio e Potássio/farmacologia
Membro 1 da Família 12 de Carreador de Soluto/antagonistas & inibidores
Membro 1 da Família 12 de Carreador de Soluto/metabolismo
Resistência Vascular/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Diuretics); 0 (Kcnj1 protein, rat); 0 (Potassium Channel Blockers); 0 (Potassium Channels, Inwardly Rectifying); 0 (Slc12a1 protein, rat); 0 (Sodium Potassium Chloride Symporter Inhibitors); 0 (Solute Carrier Family 12, Member 1); 0 (Vasoconstrictor Agents); 7LXU5N7ZO5 (Furosemide); RWP5GA015D (Potassium); SY7Q814VUP (Calcium)
[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:170224
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00662.2016


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[PMID]:28003191
[Au] Autor:Blankenstein KI; Borschewski A; Labes R; Paliege A; Boldt C; McCormick JA; Ellison DH; Bader M; Bachmann S; Mutig K
[Ad] Endereço:Department of Anatomy, Charité University Medicine, Berlin, Germany.
[Ti] Título:Calcineurin inhibitor cyclosporine A activates renal Na-K-Cl cotransporters via local and systemic mechanisms.
[So] Source:Am J Physiol Renal Physiol;312(3):F489-F501, 2017 Mar 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Calcineurin dephosphorylates nuclear factor of activated T cells transcription factors, thereby facilitating T cell-mediated immune responses. Calcineurin inhibitors are instrumental for immunosuppression after organ transplantation but may cause side effects, including hypertension and electrolyte disorders. Kidneys were recently shown to display activation of the furosemide-sensitive Na-K-2Cl cotransporter (NKCC2) of the thick ascending limb and the thiazide-sensitive Na-Cl cotransporter (NCC) of the distal convoluted tubule upon calcineurin inhibition using cyclosporin A (CsA). An involvement of major hormones like angiotensin II or arginine vasopressin (AVP) has been proposed. To resolve this issue, the effects of CsA treatment in normal Wistar rats, AVP-deficient Brattleboro rats, and cultured renal epithelial cells endogenously expressing either NKCC2 or NCC were studied. Acute administration of CsA to Wistar rats rapidly augmented phosphorylation levels of NKCC2, NCC, and their activating kinases suggesting intraepithelial activating effects. Chronic CsA administration caused salt retention and hypertension, along with stimulation of renin and suppression of renal cyclooxygenase 2, pointing to a contribution of endocrine and paracrine mechanisms at long term. In Brattleboro rats, CsA induced activation of NCC, but not NKCC2, and parallel effects were obtained in cultured cells in the absence of AVP. Stimulation of cultured thick ascending limb cells with AVP agonist restored their responsiveness to CsA. Our results suggest that the direct epithelial action of calcineurin inhibition is sufficient for the activation of NCC, whereas its effect on NKCC2 is more complex and requires concomitant stimulation by AVP.
[Mh] Termos MeSH primário: Inibidores de Calcineurina/toxicidade
Ciclosporina/toxicidade
Células Epiteliais/efeitos dos fármacos
Imunossupressores/toxicidade
Túbulos Renais Distais/efeitos dos fármacos
Alça do Néfron/efeitos dos fármacos
Membro 1 da Família 12 de Carreador de Soluto/agonistas
[Mh] Termos MeSH secundário: Animais
Arginina Vasopressina/farmacologia
Células Cultivadas
Ciclo-Oxigenase 2/metabolismo
Células Epiteliais/metabolismo
Hipertensão/induzido quimicamente
Hipertensão/metabolismo
Hipertensão/fisiopatologia
Túbulos Renais Distais/metabolismo
Túbulos Renais Distais/fisiopatologia
Alça do Néfron/metabolismo
Alça do Néfron/fisiopatologia
Masculino
Ratos Brattleboro
Ratos Wistar
Renina/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/agonistas
Membro 3 da Família 12 de Carreador de Soluto/genética
Membro 3 da Família 12 de Carreador de Soluto/metabolismo
Fatores de Tempo
Equilíbrio Hidroeletrolítico/efeitos dos fármacos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcineurin Inhibitors); 0 (Immunosuppressive Agents); 0 (Slc12a1 protein, rat); 0 (Slc12a3 protein, rat); 0 (Solute Carrier Family 12, Member 1); 0 (Solute Carrier Family 12, Member 3); 113-79-1 (Arginine Vasopressin); 83HN0GTJ6D (Cyclosporine); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs2 protein, rat); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00575.2016


  7 / 379 MEDLINE  
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[PMID]:28000888
[Au] Autor:Sun M; Ning J; Xu W; Zhang H; Zhao K; Li W; Li G; Li S
[Ad] Endereço:Department of Pediatrics, University of Oklahoma Health Sciences Center, Oklahoma, OK 73117, USA.
[Ti] Título:Genetic heterogeneity in patients with Bartter syndrome type 1.
[So] Source:Mol Med Rep;15(2):581-590, 2017 Feb.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Bartter syndrome (BS) type 1 is an autosomal recessive kidney disorder caused by loss­of­function mutations in the solute carrier family 12 member 1 (SLC12A1) gene. To date, 72 BS type 1 patients harboring SLC12A1 mutations have been documented. Of these 144 alleles studied, 68 different disease­causing mutations have been detected in 129 alleles, and no mutation was detected in the remaining 15 alleles. The mutation types included missense/nonsense mutations, splicing mutations and small insertions and deletions ranging from 1 to 4 nucleotides. A large deletion encompassing a whole exon in the SLC12A1 gene has not yet been reported. The current study initially identified an undocumented homozygous frameshift mutation (c.1833delT) by Sanger sequencing analysis of a single infant with BS type 1. However, in a subsequent analysis, the mutation was detected only in the father's DNA. Upon further investigation using a next­generation sequencing approach, a deletion in exons 14 and 15 in both the patient and patient's mother was detected. The deletion was subsequently confirmed by use of a long­range polymerase chain reaction and was determined to be 3.16 kb in size based on sequencing of the junction fragment. The results of the present study demonstrated that pathogenic variants of SLC12A1 are heterogeneous. Large deletions appear to serve an etiological role in BS type 1, and may be more prevalent than previously thought.
[Mh] Termos MeSH primário: Síndrome de Bartter/genética
Heterogeneidade Genética
Membro 1 da Família 12 de Carreador de Soluto/genética
[Mh] Termos MeSH secundário: Alelos
Síndrome de Bartter/patologia
Sequência de Bases
Hibridização Genômica Comparativa
DNA/química
DNA/isolamento & purificação
DNA/metabolismo
Análise Mutacional de DNA
Éxons
Genótipo
Seres Humanos
Reação em Cadeia da Polimerase
Polimorfismo Genético
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (SLC12A1 protein, human); 0 (Solute Carrier Family 12, Member 1); 9007-49-2 (DNA)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161222
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2016.6063


  8 / 379 MEDLINE  
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[PMID]:27748541
[Au] Autor:Breinbjerg A; Siggaard Rittig C; Gregersen N; Rittig S; Hvarregaard Christensen J
[Ad] Endereço:Department of Pediatrics, Aarhus University Hospital, Aarhus, Denmark.
[Ti] Título:A novel variant in the SLC12A1 gene in two families with antenatal Bartter syndrome.
[So] Source:Acta Paediatr;106(1):161-167, 2017 Jan.
[Is] ISSN:1651-2227
[Cp] País de publicação:Norway
[La] Idioma:eng
[Ab] Resumo:AIM: Bartter syndrome is an autosomal-recessive inherited disease in which patients present with hypokalaemia and metabolic alkalosis. We present two apparently nonrelated cases with antenatal Bartter syndrome type I, due to a novel variant in the SLC12A1 gene encoding the bumetanide-sensitive sodium-(potassium)-chloride cotransporter 2 in the thick ascending limb of the loop of Henle. METHODS: Blood samples were received from the two cases and 19 of their relatives, and deoxyribonucleic acid was extracted. The coding regions of the SLC12A1 gene were amplified using polymerase chain reaction, followed by bidirectional direct deoxyribonucleic acid sequencing. RESULTS: Each affected child in the two families was homozygous for a novel inherited variant in the SLC12A1gene, c.1614T>A. The variant predicts a change from a tyrosine codon to a stop codon (p.Tyr538Ter). The two cases presented antenatally and at six months of age, respectively. CONCLUSION: The two cases were homozygous for the same variant in the SLC12A1 gene, but presented clinically at different ages. This could eventually be explained by the presence of other gene variants or environmental factors modifying the phenotypes. The phenotypes of the patients were similar to other patients with antenatal Bartter syndrome.
[Mh] Termos MeSH primário: Síndrome de Bartter/genética
Mutação de Sentido Incorreto
Membro 1 da Família 12 de Carreador de Soluto/genética
[Mh] Termos MeSH secundário: Síndrome de Bartter/diagnóstico
Feminino
Marcadores Genéticos
Homozigoto
Seres Humanos
Lactente
Recém-Nascido
Masculino
Linhagem
Gravidez
Diagnóstico Pré-Natal
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Genetic Markers); 0 (SLC12A1 protein, human); 0 (Solute Carrier Family 12, Member 1)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE
[do] DOI:10.1111/apa.13635


  9 / 379 MEDLINE  
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[PMID]:27881573
[Au] Autor:Esbaugh AJ; Cutler B
[Ad] Endereço:University of Texas at Austin Marine Science Institute, Austin, Texas a.esbaugh@austin.utexas.edu.
[Ti] Título:Intestinal Na+, K+, 2Cl- cotransporter 2 plays a crucial role in hyperosmotic transitions of a euryhaline teleost.
[So] Source:Physiol Rep;4(22), 2016 Nov.
[Is] ISSN:2051-817X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Euryhaline fishes, such as the red drum (Sciaenops ocellatus), must quickly transition between hyperosmotic and hypoosmotic physiological strategies. When freshwater individuals transition to seawater they are exposed to increased diffusive water loss and ion gain. To maintain osmoregulatory balance these animals must drink and absorb seawater through the intestine, followed by ion excretion at the gills. The ability of fishes to transition between strategies can limit the magnitude of osmotic shock that can be tolerated. Here, we demonstrate that red drum can tolerate direct transfer from freshwater to full-strength seawater with marginal impacts on osmotic balance, as indicated by plasma and muscle ion concentration, as well as muscle water. Seawater transition is concurrent with a significant increase in intestinal fluid volume. Typical patterns of osmoregulatory plasticity were observed in the gill with increased expression of nkcc1 and cftr Expression changes in the anterior intestine were observed after 24 h for nkcc2 with smaller and later responses observed for slc26a3, slc26a6, and nbc Immunofluorescence staining demonstrated similar patterns of NKCC localization in freshwater and seawater intestines; however, reduced basolateral staining of V-type ATPase was observed in seawater. Electrophysiological preparations demonstrated that seawater fish had increased absorptive current in the anterior intestine, which was significantly reduced in the presence of 10 µmol/L bumetanide. Overall, these results suggest that nkcc2 plays a crucial role during hyperosmotic transitions, and may be a more important complement to the well-known bicarbonate secretion pathway than generally considered.
[Mh] Termos MeSH primário: Peixes/metabolismo
Brânquias/fisiologia
Intestinos/fisiologia
Osmorregulação/fisiologia
Água do Mar/efeitos adversos
Simportadores de Cloreto de Sódio-Potássio/fisiologia
Membro 2 da Família 12 de Carreador de Soluto/metabolismo
[Mh] Termos MeSH secundário: Adaptação Fisiológica
Animais
Bumetanida/administração & dosagem
Bumetanida/farmacologia
Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo
Água Doce
Expressão Gênica/genética
Brânquias/metabolismo
Absorção Intestinal/fisiologia
Intestinos/metabolismo
Transporte de Íons/fisiologia
Osmorregulação/genética
Salinidade
Inibidores de Simportadores de Cloreto de Sódio e Potássio/administração & dosagem
Inibidores de Simportadores de Cloreto de Sódio e Potássio/farmacologia
Simportadores de Cloreto de Sódio-Potássio/metabolismo
ATPase Trocadora de Sódio-Potássio/metabolismo
Membro 1 da Família 12 de Carreador de Soluto/efeitos dos fármacos
Membro 1 da Família 12 de Carreador de Soluto/metabolismo
ATPases Vacuolares Próton-Translocadoras/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Sodium Potassium Chloride Symporter Inhibitors); 0 (Sodium-Potassium-Chloride Symporters); 0 (Solute Carrier Family 12, Member 1); 0 (Solute Carrier Family 12, Member 2); 0Y2S3XUQ5H (Bumetanide); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); EC 3.6.1.- (Vacuolar Proton-Translocating ATPases); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161125
[St] Status:MEDLINE


  10 / 379 MEDLINE  
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[PMID]:27865300
[Au] Autor:Chen L; LaRocque LM; Efe O; Wang J; Sands JM; Klein JD
[Ad] Endereço:Department of Medicine, Emory University School of Medicine, Atlanta, Georgia; Department of Internal Medicine & Geriatrics, Zhongnan Hospital of Wuhan University, Wuhan, China.
[Ti] Título:Effect of Dapagliflozin Treatment on Fluid and Electrolyte Balance in Diabetic Rats.
[So] Source:Am J Med Sci;352(5):517-523, 2016 Nov.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: This study evaluates the effect of dapagliflozin, a SGLT2 inhibitor, on fluid or electrolyte balance and its effect on urea transporter-A1 (UT-A1), aquaporin-2 (AQP2) and Na-K-2Cl cotransporter (NKCC2) protein abundance in diabetic rats. METHODS: Diabetes mellitus (DM) was induced by injection of streptozotocin into the tail vein. Serum Na , K , Cl concentration, urine Na , K , Cl excretion, blood glucose, urine glucose excretion, urine volume, urine osmolality and urine urea excretion were analyzed after the administration of dapagliflozin. UT-A1, AQP2 and NKCC2 proteins were detected by western blot. RESULTS: Dapagliflozin treatment decreased blood glucose concentration by 38% at day 7 and by 47% at day 14 and increased the urinary glucose excretion rate compared with the untreated diabetic animals. Increased 24-hour urine volume, decreased urine osmolality and hyponatremia, hypokalemia and hypochloremia observed in diabetic rats were attenuated by dapagliflozin treatment. Western blot analysis showed that UT-A1, AQP2 and NKCC2 proteins are upregulated in DM rats over control rats; dapagliflozin treatment results in a further increase in inner medulla tip UT-A1 protein abundance by 42% at day 7 and by 46% at day 14, but it did not affect the DM-induced upregulation of AQP2 and NKCC2 proteins. CONCLUSION: Dapagliflozin treatment augmented the compensatory changes in medullary transport proteins in DM. These changes would tend to conserve solute and water even with persistent glycosuria. Therefore, diabetic rats treated with dapagliflozin have a mild osmotic diuresis compared to nondiabetic animals, but this does not result in an electrolyte disorder or significant volume depletion.
[Mh] Termos MeSH primário: Compostos Benzidrílicos/uso terapêutico
Diabetes Mellitus Experimental/tratamento farmacológico
Glucosídeos/uso terapêutico
Rim/efeitos dos fármacos
Transportador 2 de Glucose-Sódio/antagonistas & inibidores
Equilíbrio Hidroeletrolítico/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aquaporina 2/metabolismo
Compostos Benzidrílicos/farmacologia
Glicemia/efeitos dos fármacos
Diabetes Mellitus Experimental/metabolismo
Glucosídeos/farmacologia
Glicosúria/tratamento farmacológico
Rim/metabolismo
Masculino
Proteínas de Membrana Transportadoras/metabolismo
Ratos Sprague-Dawley
Membro 1 da Família 12 de Carreador de Soluto/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(3-(4-ethoxybenzyl)-4-chlorophenyl)-6-hydroxymethyltetrahydro-2H-pyran-3,4,5-triol); 0 (Aqp2 protein, rat); 0 (Aquaporin 2); 0 (Benzhydryl Compounds); 0 (Blood Glucose); 0 (Glucosides); 0 (Membrane Transport Proteins); 0 (Slc12a1 protein, rat); 0 (Sodium-Glucose Transporter 2); 0 (Solute Carrier Family 12, Member 1); 0 (UT-A1 protein, rat)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161121
[St] Status:MEDLINE



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