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[PMID]:29038209
[Au] Autor:Packer M
[Ad] Endereço:From Baylor Heart and Vascular Institute, Baylor University Medical Center, Dallas, TX. milton.packer@baylorhealth.edu.
[Ti] Título:Activation and Inhibition of Sodium-Hydrogen Exchanger Is a Mechanism That Links the Pathophysiology and Treatment of Diabetes Mellitus With That of Heart Failure.
[So] Source:Circulation;136(16):1548-1559, 2017 Oct 17.
[Is] ISSN:1524-4539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mechanisms underlying the progression of diabetes mellitus and heart failure are closely intertwined, such that worsening of one condition is frequently accompanied by worsening of the other; the degree of clinical acceleration is marked when the 2 coexist. Activation of the sodium-hydrogen exchanger in the heart and vasculature (NHE1 isoform) and the kidneys (NHE3 isoform) may serve as a common mechanism that links both disorders and may underlie their interplay. Insulin insensitivity and adipokine abnormalities (the hallmarks of type 2 diabetes mellitus) are characteristic features of heart failure; conversely, neurohormonal systems activated in heart failure (norepinephrine, angiotensin II, aldosterone, and neprilysin) impair insulin sensitivity and contribute to microvascular disease in diabetes mellitus. Each of these neurohormonal derangements may act through increased activity of both NHE1 and NHE3. Drugs used to treat diabetes mellitus may favorably affect the pathophysiological mechanisms of heart failure by inhibiting either or both NHE isoforms, and drugs used to treat heart failure may have beneficial effects on glucose tolerance and the complications of diabetes mellitus by interfering with the actions of NHE1 and NHE3. The efficacy of NHE inhibitors on the risk of cardiovascular events may be enhanced when heart failure and glucose intolerance coexist and may be attenuated when drugs with NHE inhibitory actions are given concomitantly. Therefore, the sodium-hydrogen exchanger may play a central role in the interplay of diabetes mellitus and heart failure, contribute to the physiological and clinical progression of both diseases, and explain certain drug-drug and drug-disease interactions that have been reported in large-scale randomized clinical trials.
[Mh] Termos MeSH primário: Proteínas de Transporte de Cátions/metabolismo
Diabetes Mellitus/metabolismo
Insuficiência Cardíaca/metabolismo
Trocadores de Sódio-Hidrogênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Fármacos Cardiovasculares/efeitos adversos
Proteínas de Transporte de Cátions/antagonistas & inibidores
Comorbidade
Diabetes Mellitus/tratamento farmacológico
Diabetes Mellitus/epidemiologia
Diabetes Mellitus/fisiopatologia
Progressão da Doença
Interações Medicamentosas
Insuficiência Cardíaca/tratamento farmacológico
Insuficiência Cardíaca/epidemiologia
Insuficiência Cardíaca/fisiopatologia
Seres Humanos
Hipoglicemiantes/efeitos adversos
Polimedicação
Fatores de Risco
Trocador 1 de Sódio-Hidrogênio
Trocador 3 de Sódio-Hidrogênio
Trocadores de Sódio-Hidrogênio/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cardiovascular Agents); 0 (Cation Transport Proteins); 0 (Hypoglycemic Agents); 0 (SLC9A1 protein, human); 0 (SLC9A3 protein, human); 0 (Sodium-Hydrogen Exchanger 1); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCULATIONAHA.117.030418


  2 / 821 MEDLINE  
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[PMID]:28768665
[Au] Autor:Hu MC; Bobulescu IA; Quiñones H; Gisler SM; Moe OW
[Ad] Endereço:Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas; Ming-Chang.Hu@UTSouthwestern.edu.
[Ti] Título:Dopamine reduces cell surface Na /H exchanger-3 protein by decreasing NHE3 exocytosis and cell membrane recycling.
[So] Source:Am J Physiol Renal Physiol;313(4):F1018-F1025, 2017 Oct 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The intrarenal autocrine-paracrine dopamine (DA) system mediates a significant fraction of the natriuresis in response to a salt load. DA inhibits a number of Na transporters to effect sodium excretion, including the proximal tubule Na /H exchanger-3 (NHE3). DA represent a single hormone that regulates NHE3 at multiple levels, including translation, degradation, endocytosis, and protein phosphorylation. Because cell surface NHE3 protein is determined by the balance between exocytotic insertion and endocytotic retrieval, we examined whether DA acutely affects the rate of NHE3 exocytosis in a cell culture model. DA inhibited NHE3 exocytosis at a dose-dependent manner with a half maximal around 10 M. The DA effect on NHE3 exocytosis was blocked by inhibition of protein kinase A and by brefeldin A, which inhibits endoplasmic reticulum-to-Golgi transport. NHE3 directly interacts with the ε-subunit of coatomer protein based on yeast-two-hybrid and coimmunoprecipitation. Because NHE3 has been shown to be recycled back to the cell membrane after endocytosis, we measured NHE3 recycling using a biochemical reinsertion assay and showed that reinsertion of NHE3 back to the membrane is also inhibited by DA. In conclusion, among the many mechanisms by which DA reduces apical membrane NHE3 and induces proximal tubule natriuresis, one additional mechanism is inhibition of exocytotic insertion and reinsertion of NHE3 in the apical cell surface.
[Mh] Termos MeSH primário: Membrana Celular/efeitos dos fármacos
Dopamina/farmacologia
Exocitose/efeitos dos fármacos
Rim/efeitos dos fármacos
Trocadores de Sódio-Hidrogênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Membrana Celular/metabolismo
Células Cultivadas
Didelphis
Relação Dose-Resposta a Droga
Regulação para Baixo
Rim/metabolismo
Natriurese/efeitos dos fármacos
Transporte Proteico
Trocador 3 de Sódio-Hidrogênio
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00251.2017


  3 / 821 MEDLINE  
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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


  4 / 821 MEDLINE  
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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


  5 / 821 MEDLINE  
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[PMID]:28506883
[Au] Autor:Godinho AN; Costa GT; Oliveira NO; Cardi BA; Uchoa DEA; Silveira ER; Quintas LEM; Noël FG; Fonteles MC; Carvalho KM; Santos CF; Lessa LMA; do Nascimento NRF
[Ad] Endereço:Biomedical Sciences Superior Institute, State University of Ceará, Fortaleza, Brazil.
[Ti] Título:Effects of cardiotonic steroids on isolated perfused kidney and NHE3 activity in renal proximal tubules.
[So] Source:Biochim Biophys Acta;1861(8):1943-1950, 2017 08.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cardiotonic steroids (CS) are known as modulators of sodium and water homeostasis. These compounds contribute to the excretion of sodium under overload conditions due to its natriuretic property related to the inhibition of the renal Na /K -ATPase (NKA) pump α1 isoform. NHE3, the main route for Na reabsorption in the proximal tubule, depends on the Na gradient generated by the NKA pump. In the present study we aimed to investigate the effects of marinobufagin (MBG) and telocinobufagin (TBG) on the renal function of isolated perfused rat kidney and on the inhibition of NKA activity. Furthermore, we investigated the mechanisms for the cardiotonic steroid-mediated natriuretic effect, by evaluating and comparing the effects of bufalin (BUF), ouabain (OUA), MBG and TBG on NHE3 activity in the renal proximal tubule in vivo. TBG significantly increased GFR, UF, natriuresis and kaliuresis in isolated perfused rat kidney, and inhibits the activity of NKA at a much higher rate than MBG. By stationary microperfusion technique, the perfusion with BUF, OUA, TBG or MBG promoted an inhibitory effect on NHE3 activity, whereas BUF was the most effective agent, and demonstrated a dose-dependent response, with maximal inhibition at 50nM. Furthermore, our data showed the role of NKA-Src kinase pathway in the inhibition of NHE3 by CS. Finally, a downstream step, MEK1/2-ERK1/2 was also investigated, and, similar to Src inhibition, the MEK1/2 inhibitor (U0126) suppressed the BUF effect. Our findings indicate the involvement of NKA-SRc-Kinase-Ras-Raf-ERK1/2 pathway in the downregulation of NHE3 by cardiotonic steroids in the renal proximal tubule, promoting a reduction of proximal sodium reabsorption and natriuresis.
[Mh] Termos MeSH primário: Bufanolídeos/farmacologia
Túbulos Renais Proximais/efeitos dos fármacos
Rim/efeitos dos fármacos
Trocadores de Sódio-Hidrogênio/metabolismo
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
MAP Quinases Reguladas por Sinal Extracelular/fisiologia
Técnicas In Vitro
Túbulos Renais Proximais/metabolismo
Masculino
Ratos
Ratos Wistar
Trocador 3 de Sódio-Hidrogênio
ATPase Trocadora de Sódio-Potássio/antagonistas & inibidores
ATPase Trocadora de Sódio-Potássio/fisiologia
Quinases da Família src/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bufanolides); 0 (Slc9a3 protein, rat); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); 3KBT25GV2B (marinobufagenin); 472-26-4 (telocinobufagin); EC 2.7.10.2 (src-Family Kinases); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE


  6 / 821 MEDLINE  
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[PMID]:28495802
[Au] Autor:Yin J; Tse CM; Cha B; Sarker R; Zhu XC; Walentinsson A; Greasley PJ; Donowitz M
[Ad] Endereço:Department of Medicine, Division of Gastroenterology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
[Ti] Título:A common NHE3 single-nucleotide polymorphism has normal function and sensitivity to regulatory ligands.
[So] Source:Am J Physiol Gastrointest Liver Physiol;313(2):G129-G137, 2017 Aug 01.
[Is] ISSN:1522-1547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Na /H exchanger NHE3 mediates the majority of intestinal and renal electroneutral sodium absorption. Dysfunction of NHE3 is associated with a variety of diarrheal diseases. We previously reported that the NHE3 gene ( ) has more than 400 single-nucleotide polymorphisms (SNPs) but few nonsynonymous polymorphisms. Among the latter, one polymorphism (rs2247114-G>A), which causes a substitution from arginine to cysteine at amino acid position 799 (p.R799C), is common in Asian populations. To improve our understanding of the population distribution and potential clinical significance of the NHE3-799C variant, we investigated the frequency of this polymorphism in different ethnic groups using bioinformatics analyses and in a cohort of Japanese patients with cardiovascular or renal disease. We also characterized the function of human NHE3-799C and its sensitivity to regulatory ligands in an in vitro model. NHE3-799C had an allele frequency of 29.5-57.6% in Asian populations, 11.1-23.6% in European populations, and 10.2-22.7% in African populations. PS120/FLAG-NHERF2 fibroblasts stably expressing NHE3-799C had lower total protein expression but a higher percentage of surface expression than those expressing NHE3-799R. NHE3-799C had similar basal activity to NHE3-799R and was similarly stimulated or inhibited, by serum or forskolin, respectively. Tenapanor, a small-molecule NHE3 inhibitor, dose-dependently inhibited NHE3-799R and NHE3-799C activities. The IC values of tenapanor for NHE3-799C and NHE3-799R were significantly different, but both were in the nanomolar range. These results suggest that NHE3-799C is a common variant enriched in Asian populations, is not associated with compromised function or abnormal regulation, and is unlikely to contribute to clinical disease. This study reports results on the functional significance of human NHE3-799C under basal conditions and in response to regulatory ligands, including a novel NHE3 inhibitor called tenapanor. We demonstrate that NHE3-799C is a common variant of NHE3 that is enriched in Asian populations; however, in contrast to our previous studies using rabbit NHE3, its presence seems to have limited clinical significance in humans and is not associated with compromised function or abnormal transport regulation.
[Mh] Termos MeSH primário: Alelos
Frequência do Gene
Polimorfismo de Nucleotídeo Único
Trocadores de Sódio-Hidrogênio/genética
[Mh] Termos MeSH secundário: Grupo com Ancestrais do Continente Asiático/genética
Doenças Cardiovasculares/genética
Biologia Computacional
Grupo com Ancestrais do Continente Europeu/genética
Genótipo
Seres Humanos
Nefropatias/genética
Mutação
Trocador 3 de Sódio-Hidrogênio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (SLC9A3 protein, human); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers)
[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:170513
[St] Status:MEDLINE
[do] DOI:10.1152/ajpgi.00044.2017


  7 / 821 MEDLINE  
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Malnic, Gerhard
Texto completo
[PMID]:28490531
[Au] Autor:Castelo-Branco RC; Leite-Dellova DCA; Fernandes FB; Malnic G; de Mello-Aires M
[Ad] Endereço:Department of Physiology and Biophysics, Biomedical Sciences Institute, University of São Paulo, São Paulo, Brazil; regianebranco@hotmail.com.
[Ti] Título:The effects of angiotensin-(1-7) on the exchanger NHE3 and on [Ca ] in the proximal tubules of spontaneously hypertensive rats.
[So] Source:Am J Physiol Renal Physiol;313(2):F450-F460, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The acute effects of angiotensin-1-7 [ANG-(1-7)] on the reabsorptive bicarbonate flow (J[Formula: see text]) were evaluated using stationary microperfusion in vivo in the proximal tubules of spontaneously hypertensive rats (SHR) and their normotensive controls, Wistar-Kyoto (WKY) rats, using a microelectrode sensitive to H In WKY rats, the control J[Formula: see text] was 2.40 ± 0.10 nmol·cm ·s ( = 120); losartan (10 M) or A779 (10 M, a specific Mas antagonist), alone or in combination with losartan, decreased the J[Formula: see text] ANG-(1-7) had biphasic effects on J[Formula: see text]: at 10 M, it inhibited, and at 10 , it stimulated the flow. S3226 [10 M, a specific Na -H exchanger 3 (NHE3) antagonist] decreased J[Formula: see text] and changed the stimulatory effect of ANG-(1-7) to an inhibitory one but did not alter the inhibitory action of ANG-(1-7). In SHR, the control J[Formula: see text] was 2.04 ± 0.13 nmol·cm ·s ( = 56), and A779 and/or losartan reduced the flow. ANG-(1-7) at 10 M increased J[Formula: see text], and ANG-(1-7) at 10 M reduced it. The effects of A779, losartan, and S3226 on the J[Formula: see text] were similar to those found in WKY rats, which indicated that in SHR, the ANG-(1-7) action on the NHE3 was via Mas and ANG II type 1. The cytosolic calcium in the WKY or SHR rats was ~100 nM and was increased by ANG-(1-7) at 10 or 10 M. In hypertensive animals, a high plasma level of ANG-(1-7) inhibited NHE3 in the proximal tubule, which mitigated the hypertension caused by the high plasma level of ANG II.
[Mh] Termos MeSH primário: Angiotensina I/farmacologia
Bicarbonatos/metabolismo
Pressão Sanguínea/efeitos dos fármacos
Cálcio/metabolismo
Hipertensão/metabolismo
Túbulos Renais Proximais/efeitos dos fármacos
Fragmentos de Peptídeos/farmacologia
Trocadores de Sódio-Hidrogênio/antagonistas & inibidores
[Mh] Termos MeSH secundário: Angiotensina II/metabolismo
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Animais
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Hipertensão/fisiopatologia
Túbulos Renais Proximais/metabolismo
Túbulos Renais Proximais/fisiopatologia
Masculino
Proteínas Proto-Oncogênicas/agonistas
Proteínas Proto-Oncogênicas/metabolismo
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Receptores Acoplados a Proteínas-G/agonistas
Receptores Acoplados a Proteínas-G/metabolismo
Reabsorção Renal/efeitos dos fármacos
Trocador 3 de Sódio-Hidrogênio
Trocadores de Sódio-Hidrogênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Bicarbonates); 0 (Peptide Fragments); 0 (Proto-Oncogene Proteins); 0 (Receptors, G-Protein-Coupled); 0 (Slc9a3 protein, rat); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); 0 (proto-oncogene proteins c-mas-1); 11128-99-7 (Angiotensin II); 9041-90-1 (Angiotensin I); IJ3FUK8MOF (angiotensin I (1-7)); SY7Q814VUP (Calcium)
[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:170512
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00557.2016


  8 / 821 MEDLINE  
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[PMID]:28438314
[Au] Autor:Zhou X; Packialakshmi B; Xiao Y; Nurmukhambetova S; Lees JR
[Ad] Endereço:Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, MD, United States. Electronic address: xiaoming.zhou@usuhs.edu.
[Ti] Título:Progression of experimental autoimmune encephalomyelitis is associated with up-regulation of major sodium transporters in the mouse kidney cortex under a normal salt diet.
[So] Source:Cell Immunol;317:18-25, 2017 Jul.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Recent demonstrations of exacerbation of experimental autoimmune encephalomyelitis (EAE) by high salt diets prompted us to study whether EAE stimulated Na absorption by the renal cortex, a primary regulatory site for Na balance, even under a normal NaCl diet. We found that as EAE progressed from mild to severe symptoms, there were parallel increases in the protein abundance of NHE3 and αENaC and the Na,K-ATPase activity with an affiliated elevation of its ß1-subunit protein. These effects are associated with increases in the protein levels of the well-known regulators SGK1 and scaffold NHERF2, and phosphorylation of ERK1/2. These effects of EAE could not be explained by reduction in water or food intake. We conclude that EAE progression is associated with up-regulation of major Na transporters, which is most likely driven by increased expression of SGK1 and NHERF2 and activation of ERK1/2. These data suggest that EAE progression increases Na absorption by the renal cortex.
[Mh] Termos MeSH primário: Encefalomielite Autoimune Experimental/imunologia
Rim/metabolismo
Esclerose Múltipla/imunologia
[Mh] Termos MeSH secundário: Animais
Dieta
Progressão da Doença
Canais Epiteliais de Sódio/genética
Canais Epiteliais de Sódio/metabolismo
Feminino
Seres Humanos
Proteínas Imediatamente Precoces/genética
Proteínas Imediatamente Precoces/metabolismo
Rim/imunologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Glicoproteína Mielina-Oligodendrócito/imunologia
Fragmentos de Peptídeos/imunologia
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
Cloreto de Sódio
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
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epithelial Sodium Channels); 0 (Immediate-Early Proteins); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (Phosphoproteins); 0 (SLC9A3 protein, human); 0 (Slc9a3 protein, mouse); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); 0 (myelin oligodendrocyte glycoprotein (35-55)); 0 (sodium-hydrogen exchanger regulatory factor); 451W47IQ8X (Sodium Chloride); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (serum-glucocorticoid regulated kinase); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase)
[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:170426
[St] Status:MEDLINE


  9 / 821 MEDLINE  
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[PMID]:28384194
[Au] Autor:Wang YY; Lin YH; Wu YN; Chen YL; Lin YC; Cheng CY; Chiang HS
[Ad] Endereço:Department of Chemistry, Fu Jen Catholic University, New Taipei City, Taiwan.
[Ti] Título:Loss of SLC9A3 decreases CFTR protein and causes obstructed azoospermia in mice.
[So] Source:PLoS Genet;13(4):e1006715, 2017 Apr.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene cause cystic fibrosis (CF) and are associated with congenital bilateral absence of the vas deferens (CBAVD), which is the major cause of infertility in male patients with CF. However, most Taiwanese patients with CBAVD do not carry major CFTR mutations. Some patients have a single copy deletion of the solute carrier family 9 isoform 3 (SLC9A3) gene. SLC9A3 is a Na+/H+ exchanger, and depleted Slc9a3 in male mice causes infertility due to the abnormal dilated lumen of the rete testis and efferent ductules. Furthermore, SLC9A3 interacts with CFTR in the pancreatic duct and functions as a genetic modifier of CF. However, SLC9A3 function and its relation to CFTR expression in the male reproductive tract in vivo remain elusive. In the present study, we found that CFTR expression was dramatically decreased in the epididymis and vas deferens of Slc9a3 knockout mice. Adult Slc9a3-/- mice showed not only significantly decreased epididymis and vas deferens weight but also increased testis weight. Furthermore, Slc9a3-/- mice developed obstructive azoospermia because of abnormal abundant secretions and calcification in the lumen of the reproductive tract. Ultrastructural analysis of the epithelium in Slc9a3-/-epididymis and vas deferens displayed disorganized and reduced number of stereocilia and numerous secretory apparatuses. Our data revealed that interdependence between SLC9A3 and CFTR is critical for maintaining a precise microenvironment in the epithelial cytoarchitecture of the male reproductive tract. The Slc9a3-deficient mice with impaired male excurrent ducts in this study provide proof for our clinical findings that some Taiwanese of CBAVD carry SLC9A3 deletion but without major CFTR mutations.
[Mh] Termos MeSH primário: Regulador de Condutância Transmembrana em Fibrose Cística/biossíntese
Infertilidade Masculina/genética
Oligospermia/genética
Infecções Respiratórias/genética
Trocadores de Sódio-Hidrogênio/genética
[Mh] Termos MeSH secundário: Animais
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Regulação da Expressão Gênica no Desenvolvimento
Seres Humanos
Infertilidade Masculina/patologia
Masculino
Camundongos
Camundongos Knockout
Mutação
Oligospermia/patologia
Ductos Pancreáticos/metabolismo
Ductos Pancreáticos/patologia
Infecções Respiratórias/patologia
Trocador 3 de Sódio-Hidrogênio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (SLC9A3 protein, human); 0 (Slc9a3 protein, mouse); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
[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:170407
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006715


  10 / 821 MEDLINE  
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[PMID]:28283572
[Au] Autor:Cha B; Yang J; Singh V; Zachos NC; Sarker RI; Chen TE; Chakraborty M; Tse CM; Donowitz M
[Ad] Endereço:From the Departments of Physiology and Medicine, Gastroenterology Division, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
[Ti] Título:PDZ domain-dependent regulation of NHE3 protein by both internal Class II and C-terminal Class I PDZ-binding motifs.
[So] Source:J Biol Chem;292(20):8279-8290, 2017 May 19.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NHE3 directly binds Na /H exchanger regulatory factor (NHERF) family scaffolding proteins that are required for many aspects of NHE3 regulation. The NHERFs bind both to an internal region (amino acids 586-660) of the NHE3 C terminus and to the NHE3 C-terminal four amino acids. The internal NHERF-binding region contains both putative Class I (- SAV-) and Class II (- CLDM-) PDZ-binding motifs (PBMs). Point mutagenesis showed that only the Class II motif contributes to NHERF binding. In this study, the roles in regulation of NHE3 activity of these two PBMs were investigated, revealing the following findings. 1) Interaction occurred between these binding sites because mutation of either removed nearly all NHERF binding. 2) Mutations in either significantly reduced basal NHE3 activity. Total and percent plasma membrane (PM) NHE3 protein expression was reduced in the C-terminal but not in the internal PBD mutation. 3) cGMP- and Ca -mediated inhibition of NHE3 was impaired in both the internal and the C-terminal PBM mutations. 4) There was a significant reduction in half-life of the PM pool of NHE3 in only the internal PBM mutation but no change in total NHE3 half-life in either. 5) There were some differences in NHE3-associating proteins in the two PBM mutations. In conclusion, NHE3 binds to NHERF proteins via both an internal Class II PBM and C-terminal Class I PBM, which interact. The former determines NHE3 stability in the PM, and the latter determines total expression and percent PM expression.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Membrana Celular/metabolismo
GMP Cíclico/metabolismo
Fosfoproteínas/metabolismo
Trocadores de Sódio-Hidrogênio/metabolismo
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Linhagem Celular
Membrana Celular/genética
GMP Cíclico/genética
Seres Humanos
Mutação
Domínios PDZ
Fosfoproteínas/genética
Ligação Proteica/fisiologia
Estabilidade Proteica
Trocador 3 de Sódio-Hidrogênio
Trocadores de Sódio-Hidrogênio/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phosphoproteins); 0 (SLC9A3 protein, human); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); 0 (sodium-hydrogen exchanger regulatory factor); H2D2X058MU (Cyclic GMP); SY7Q814VUP (Calcium)
[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:170312
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.774489



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