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[PMID]:28468962
[Au] Autor:Gohar EY; Kasztan M; Becker BK; Speed JS; Pollock DM
[Ad] Endereço:Cardio-Renal Physiology & Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
[Ti] Título:Ovariectomy uncovers purinergic receptor activation of endothelin-dependent natriuresis.
[So] Source:Am J Physiol Renal Physiol;313(2):F361-F369, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We recently reported that natriuresis produced by renal medullary salt loading is dependent on endothelin (ET)-1 and purinergic (P2) receptors in male rats. Because sex differences in ET-1 and P2 signaling have been reported, we decided to test whether ovarian sex hormones regulate renal medullary ET-1 and P2-dependent natriuresis. The effect of medullary NaCl loading on Na excretion was determined in intact and ovariectomized (OVX) female Sprague-Dawley rats with and without ET-1 or P2 receptor antagonism. Isosmotic saline (284 mosmol/kgH O) was infused in the renal medullary interstitium of anesthetized rats during a baseline urine collection period, followed by isosmotic or hyperosmotic saline (1,800 mosmol/kgH O) infusion. Medullary NaCl loading significantly enhanced Na excretion in intact and OVX female rats. ET or P2 receptor blockade did not attenuate the natriuretic effect of medullary NaCl loading in intact females, whereas ET or P2 receptor blockade attenuated the natriuretic response to NaCl loading in OVX rats. Activation of medullary P2Y and P2Y receptors by UTP infusion had no significant effect in intact females but enhanced Na excretion in OVX rats. Combined ET receptor blockade significantly inhibited the natriuretic response to UTP observed in OVX rats. These data demonstrate that medullary NaCl loading induces ET-1 and P2-independent natriuresis in intact females. In OVX, activation of medullary P2 receptors promotes ET-dependent natriuresis, suggesting that ovarian hormones may regulate the interplay between the renal ET-1 and P2 signaling systems to facilitate Na excretion.
[Mh] Termos MeSH primário: Endotelina-1/metabolismo
Medula Renal/metabolismo
Natriurese
Ovariectomia
Receptores Purinérgicos P2Y2/metabolismo
Receptores Purinérgicos P2/metabolismo
Eliminação Renal
Sódio/urina
[Mh] Termos MeSH secundário: Animais
Antagonistas dos Receptores de Endotelina/farmacologia
Endotelina-1/genética
Feminino
Medula Renal/efeitos dos fármacos
Natriurese/efeitos dos fármacos
Agonistas do Receptor Purinérgico P2/farmacologia
Antagonistas do Receptor Purinérgico P2/farmacologia
Ratos Sprague-Dawley
Receptores Purinérgicos P2/efeitos dos fármacos
Receptores Purinérgicos P2Y2/efeitos dos fármacos
Eliminação Renal/efeitos dos fármacos
Transdução de Sinais
Cloreto de Sódio/administração & dosagem
Cloreto de Sódio/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists); 0 (Endothelin-1); 0 (P2ry2 protein, rat); 0 (Purinergic P2 Receptor Agonists); 0 (Purinergic P2 Receptor Antagonists); 0 (Receptors, Purinergic P2); 0 (Receptors, Purinergic P2Y2); 0 (purinoceptor P2Y4); 451W47IQ8X (Sodium Chloride); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00098.2017


  2 / 8516 MEDLINE  
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[PMID]:28827476
[Au] Autor:Patel SN; Ali Q; Samuel P; Steckelings UM; Hussain T
[Ad] Endereço:From the Department of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, TX (S.N.P., Q.A., P.S., T.H.); and Department of Cardiovascular and Renal Research, Institute of Molecular Medicine, University of Southern Denmark, Odense (U.M.S.).
[Ti] Título:Angiotensin II Type 2 Receptor and Receptor Mas Are Colocalized and Functionally Interdependent in Obese Zucker Rat Kidney.
[So] Source:Hypertension;70(4):831-838, 2017 Oct.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The actions of angiotensin II type 2 receptor (AT R) and the receptor Mas (MasR) are complex but show similar pronatriuretic function; particularly, AT R expression and natriuretic function are enhanced in obese/diabetic rat kidney. In light of some reports suggesting a potential positive interaction between these receptors, we tested hypothesis that renal AT R and MasR physically interact and are interdependent to stimulate cell signaling and promote natriuresis in obese rats. We found that infusion of AT R agonist C21 in obese Zucker rats (OZR) increased urine flow and urinary Na excretion which were attenuated by simultaneous infusion of the AT R antagonist PD123319 or the MasR antagonist A-779. Similarly, infusion of MasR agonist Ang-(1-7) in OZR increased urine flow and urinary Na excretion, which were attenuated by simultaneous infusion of A-779 or PD123319. Experiment in isolated renal proximal tubules of OZR revealed that both the agonists C21 and Ang-(1-7) stimulated NO which was blocked by either of the receptor antagonists. Dual labeling of AT R and MasR in OZR kidney sections and human proximal tubule epithelial cells showed that AT R and MasR are colocalized. The AT R also coimmunoprecipitated with MasR in cortical homogenate of OZR. Immunoblotting of cortical homogenate cross-linked with zero-length oxidative (sulfhydryl groups) cross-linker cupric-phenanthroline revealed a shift of AT R and MasR bands upward with overlapping migration for their complexes which were sensitive to the reducing ß-mercaptoethanol, suggesting involvement of -SH groups in cross-linking. Collectively, the study reveals that AT R and MasR are colocalized and functionally interdependent in terms of stimulating NO and promoting diuretic/natriuretic response.
[Mh] Termos MeSH primário: Pressão Sanguínea
Rim
Natriurese
Óxido Nítrico/metabolismo
Obesidade
Proteínas Proto-Oncogênicas/metabolismo
Receptor Tipo 2 de Angiotensina/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Angiotensina II/agonistas
Angiotensina II/análogos & derivados
Angiotensina II/metabolismo
Angiotensina II/farmacologia
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Bloqueadores do Receptor Tipo 2 de Angiotensina II/farmacologia
Animais
Pressão Sanguínea/efeitos dos fármacos
Pressão Sanguínea/fisiologia
Imidazóis/farmacologia
Rim/efeitos dos fármacos
Rim/metabolismo
Rim/fisiopatologia
Túbulos Renais Proximais/efeitos dos fármacos
Túbulos Renais Proximais/metabolismo
Proteínas de Membrana/metabolismo
Natriurese/efeitos dos fármacos
Natriurese/fisiologia
Obesidade/metabolismo
Obesidade/fisiopatologia
Fragmentos de Peptídeos/farmacologia
Piridinas/farmacologia
Ratos
Ratos Zucker
Vasoconstritores/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (7-Ala-angiotensin (1-7)); 0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensin II Type 2 Receptor Blockers); 0 (Imidazoles); 0 (Membrane Proteins); 0 (Peptide Fragments); 0 (Proto-Oncogene Proteins); 0 (Pyridines); 0 (Receptor, Angiotensin, Type 2); 0 (Receptors, G-Protein-Coupled); 0 (Vasoconstrictor Agents); 0 (proto-oncogene proteins c-mas-1); 11128-99-7 (Angiotensin II); 130663-39-7 (PD 123319); 31C4KY9ESH (Nitric Oxide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09679


  3 / 8516 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


  4 / 8516 MEDLINE  
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[PMID]:28768662
[Au] Autor:Ahmad A; Daneva Z; Li G; Dempsey SK; Li N; Poklis JL; Lichtman A; Li PL; Ritter JK
[Ad] Endereço:Department of Pharmacology and Toxicology, Virginia Commonwealth University School of Medicine, Richmond, Virginia.
[Ti] Título:Stimulation of diuresis and natriuresis by renomedullary infusion of a dual inhibitor of fatty acid amide hydrolase and monoacylglycerol lipase.
[So] Source:Am J Physiol Renal Physiol;313(5):F1068-F1076, 2017 Nov 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The renal medulla, considered critical for the regulation of salt and water balance and long-term blood pressure control, is enriched in anandamide and two of its major metabolizing enzymes, cyclooxygenase-2 (COX-2) and fatty acid amide hydrolase (FAAH). Infusion of anandamide (15, 30, and 60 nmol·min ·kg ) into the renal medulla of C57BL/6J mice stimulated diuresis and salt excretion in a COX-2- but not COX-1-dependent manner. To determine whether endogenous endocannabinoids in the renal medulla can elicit similar effects, the effects of intramedullary isopropyl dodecyl fluorophosphate (IDFP), which inhibits the two major endocannabinoid hydrolases, were studied. IDFP treatment increased the urine formation rate and sodium excretion in a COX-2- but not COX-1-dependent manner. Neither anandamide nor IDFP affected the glomerular filtration rate. Neither systemic (0.625 mg·kg ·30 min iv) nor intramedullary (15 nmol·min ·kg ·30 min ) IDFP pretreatment before intramedullary anandamide (15-30 nmol·min ·kg ) strictly blocked effects of anandamide, suggesting that hydrolysis of anandamide was not necessary for its diuretic effect. Intramedullary IDFP had no effect on renal blood flow but stimulated renal medullary blood flow. The effects of IDFP on urine flow rate and medullary blood flow were FAAH-dependent as demonstrated using FAAH knockout mice. Analysis of mouse urinary PGE concentrations by HPLC-electrospray ionization tandem mass spectrometry showed that IDFP treatment decreased urinary PGE These data are consistent with a role of FAAH and endogenous anandamide acting through a COX-2-dependent metabolite to regulate diuresis and salt excretion in the mouse kidney.
[Mh] Termos MeSH primário: Amidoidrolases/antagonistas & inibidores
Diurese
Inibidores Enzimáticos/farmacologia
Monoacilglicerol Lipases/antagonistas & inibidores
[Mh] Termos MeSH secundário: Amidoidrolases/metabolismo
Animais
Ácidos Araquidônicos/metabolismo
Ciclo-Oxigenase 2/metabolismo
Diurese/efeitos dos fármacos
Endocanabinoides/metabolismo
Medula Renal/efeitos dos fármacos
Medula Renal/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Monoacilglicerol Lipases/metabolismo
Natriurese/efeitos dos fármacos
Natriurese/fisiologia
Alcamidas Poli-Insaturadas/metabolismo
Circulação Renal/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Endocannabinoids); 0 (Enzyme Inhibitors); 0 (Polyunsaturated Alkamides); EC 1.14.99.- (Ptgs2 protein, mouse); EC 1.14.99.1 (Cyclooxygenase 2); EC 3.1.1.23 (Monoacylglycerol Lipases); EC 3.5.- (Amidohydrolases); EC 3.5.1.- (fatty-acid amide hydrolase); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00196.2017


  5 / 8516 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


  6 / 8516 MEDLINE  
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[PMID]:28507171
[Au] Autor:Hunter RW; Moorhouse R; Farrah TE; MacIntyre IM; Asai T; Gallacher PJ; Kerr D; Melville V; Czopek A; Morrison EE; Ivy JR; Dear JW; Bailey MA; Goddard J; Webb DJ; Dhaun N
[Ad] Endereço:From the British Heart Foundation Centre of Research Excellence and The Queen's Medical Research Institute, University of Edinburgh, United Kingdom.
[Ti] Título:First-in-Man Demonstration of Direct Endothelin-Mediated Natriuresis and Diuresis.
[So] Source:Hypertension;70(1):192-200, 2017 Jul.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endothelin (ET) receptor antagonists are potentially novel therapeutic agents in chronic kidney disease and resistant hypertension, but their use is complicated by sodium and water retention. In animal studies, this side effect arises from ET receptor blockade in the renal tubule. Previous attempts to determine whether this mechanism operates in humans have been confounded by the hemodynamic consequences of ET receptor stimulation/blockade. We aimed to determine the effects of ET signaling on salt transport in the human nephron by administering subpressor doses of the ET-1 precursor, big ET-1. We conducted a 2-phase randomized, double-blind, placebo-controlled crossover study in 10 healthy volunteers. After sodium restriction, subjects received either intravenous placebo or big ET-1, in escalating dose (≤300 pmol/min). This increased plasma concentration and urinary excretion of ET-1. Big ET-1 reduced heart rate (≈8 beats/min) but did not otherwise affect systemic hemodynamics or glomerular filtration rate. Big ET-1 increased the fractional excretion of sodium (from 0.5 to 1.0%). It also increased free water clearance and tended to increase the abundance of the sodium-potassium-chloride cotransporter (NKCC2) in urinary extracellular vesicles. Our protocol induced modest increases in circulating and urinary ET-1. Sodium and water excretion increased in the absence of significant hemodynamic perturbation, supporting a direct action of ET-1 on the renal tubule. Our data also suggest that sodium reabsorption is stimulated by ET-1 in the thick ascending limb and suppressed in the distal renal tubule. Fluid retention associated with ET receptor antagonist therapy may be circumvented by coprescribing potassium-sparing diuretics.
[Mh] Termos MeSH primário: Endotelina-1
Insuficiência Renal Crônica
Sódio/metabolismo
[Mh] Termos MeSH secundário: Adulto
Animais
Diurese/efeitos dos fármacos
Diurese/fisiologia
Método Duplo-Cego
Antagonistas dos Receptores de Endotelina/administração & dosagem
Antagonistas dos Receptores de Endotelina/efeitos adversos
Antagonistas dos Receptores de Endotelina/farmacocinética
Endotelina-1/administração & dosagem
Endotelina-1/efeitos adversos
Endotelina-1/farmacocinética
Feminino
Taxa de Filtração Glomerular
Seres Humanos
Túbulos Renais/metabolismo
Túbulos Renais/fisiopatologia
Masculino
Natriurese/efeitos dos fármacos
Natriurese/fisiologia
Receptores de Endotelina/metabolismo
Insuficiência Renal Crônica/tratamento farmacológico
Insuficiência Renal Crônica/metabolismo
Insuficiência Renal Crônica/fisiopatologia
Resultado do Tratamento
Equilíbrio Hidroeletrolítico/efeitos dos fármacos
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists); 0 (Endothelin-1); 0 (Receptors, Endothelin); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.116.08832


  7 / 8516 MEDLINE  
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[PMID]:28493961
[Au] Autor:Molina-Jijón E; Rodríguez-Muñoz R; González-Ramírez R; Namorado-Tónix C; Pedraza-Chaverri J; Reyes JL
[Ad] Endereço:Department of Physiology, Biophysics and Neuroscience, Center for Research and Advanced Studies of the National Polytechnic Institute (CINVESTAV-IPN), Mexico City, México.
[Ti] Título:Aldosterone signaling regulates the over-expression of claudin-4 and -8 at the distal nephron from type 1 diabetic rats.
[So] Source:PLoS One;12(5):e0177362, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hyperglycemia in diabetes alters tight junction (TJ) proteins in the kidney. We evaluated the participation of aldosterone (ALD), and the effect of spironolactone (SPL), a mineralocorticoid receptor antagonist, on the expressions of claudin-2, -4, -5 and -8, and occludin in glomeruli, proximal and distal tubules isolated from diabetic rats. Type 1 diabetes was induced in female Wistar rats by a single tail vein injection of streptozotocin (STZ), and SPL was administrated daily by gavage, from days 3-21. Twenty-one days after STZ injection the rats were sacrificed. In diabetic rats, the serum ALD levels were increased, and SPL-treatment did not have effect on these levels or in hyperglycemia, however, proteinuria decreased in SPL-treated diabetic rats. Glomerular damage, evaluated by nephrin and Wilm's tumor 1 (WT1) protein expressions, and proximal tubular damage, evaluated by kidney injury molecule 1 (Kim-1) and heat shock protein 72 kDa (Hsp72) expressions, were ameliorated by SPL. Also, SPL prevented decrement in claudin-5 in glomeruli, and claudin-2 and occludin in proximal tubules by decreasing oxidative stress, evaluated by superoxide anion (O2●-) production, and oxidative stress markers. In distal tubules, SPL ameliorated increase in mRNA, protein expression, and phosphorylation in threonine residues of claudin-4 and -8, through a serum and glucocorticoid-induced kinase 1 (SGK1), and with-no-lysine kinase 4 (WNK4) signaling pathway. In conclusion, this is the first study that demonstrates that ALD modulates the expression of renal TJ proteins in diabetes, and that the blockade of its actions with SPL, may be a promising therapeutic strategy to prevent alterations of TJ proteins in diabetic nephropathy.
[Mh] Termos MeSH primário: Aldosterona/metabolismo
Claudina-4/metabolismo
Claudinas/metabolismo
Diabetes Mellitus Experimental/metabolismo
Diabetes Mellitus Tipo 1/metabolismo
Néfrons/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Diabetes Mellitus Experimental/sangue
Diabetes Mellitus Experimental/complicações
Diabetes Mellitus Experimental/patologia
Diabetes Mellitus Tipo 1/sangue
Diabetes Mellitus Tipo 1/complicações
Diabetes Mellitus Tipo 1/patologia
Feminino
Hiperglicemia/sangue
Hiperglicemia/tratamento farmacológico
Hiperglicemia/prevenção & controle
Proteínas Imediatamente Precoces/metabolismo
Glomérulos Renais/efeitos dos fármacos
Glomérulos Renais/patologia
Túbulos Renais/efeitos dos fármacos
Túbulos Renais/patologia
Modelos Biológicos
Natriurese/efeitos dos fármacos
Estresse Oxidativo/efeitos dos fármacos
Fosforilação/efeitos dos fármacos
Potássio/sangue
Proteínas Serina-Treonina Quinases/metabolismo
Proteinúria/sangue
Proteinúria/complicações
Proteinúria/tratamento farmacológico
Proteinúria/prevenção & controle
Ratos Wistar
Transdução de Sinais/efeitos dos fármacos
Espironolactona/farmacologia
Espironolactona/uso terapêutico
Junções Íntimas/efeitos dos fármacos
Junções Íntimas/metabolismo
Perda de Peso/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Claudin-4); 0 (Claudins); 0 (Immediate-Early Proteins); 0 (claudin 8); 27O7W4T232 (Spironolactone); 4964P6T9RB (Aldosterone); EC 2.7.1.- (Prkwnk4 protein, rat); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (serum-glucocorticoid regulated kinase); RWP5GA015D (Potassium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177362


  8 / 8516 MEDLINE  
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[PMID]:28490529
[Au] Autor:Rosenbaek JB; Al Therwani S; Jensen JM; Mose FH; Wandall-Frostholm C; Pedersen EB; Bech JN
[Ad] Endereço:University Clinic in Nephrology and Hypertension, Regional Hospital West Jutland and Aarhus University, Aarhus, Denmark; and jepros@rm.dk.
[Ti] Título:Effect of sodium nitrite on renal function and sodium and water excretion and brachial and central blood pressure in healthy subjects: a dose-response study.
[So] Source:Am J Physiol Renal Physiol;313(2):F378-F387, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sodium nitrite (NaNO ) is converted to nitric oxide (NO) in vivo and has vasodilatory and natriuretic effects. Our aim was to examine the effects of NaNO on hemodynamics, sodium excretion, and glomerular filtration rate (GFR). In a single-blinded, placebo-controlled, crossover study, we infused placebo (0.9% NaCl) or 0.58, 1.74, or 3.48 µmol NaNO ·kg ·h for 2 h in 12 healthy subjects, after 4 days of a standard diet. Subjects were supine and water loaded. We measured brachial and central blood pressure (BP), plasma concentrations of renin, angiotensin II, aldosterone, arginine vasopressin (P-AVP), and plasma nitrite (P-[Formula: see text]), GFR by Cr-EDTA clearance, fractional excretion of sodium (FE ) free water clearance (C ), and urinary excretion rate of guanosine 3',5'-cyclic monophosphate (U-cGMP). The highest dose reduced brachial systolic BP (5.6 mmHg, = 0.003), central systolic BP (5.6 mmHg, = 0.035), and C (maximum change from 3.79 to 1.27 ml/min, = 0.031) and increased P-[Formula: see text] (from 0.065 to 0.766 µmol/l, < 0.001), while reducing U-cGMP (from 444 to 247 pmol/min, = 0.004). GFR, FE , P-AVP, and the components in the renin-angiotensin-aldosterone system did not change significantly. In conclusion, intravenous NaNO induced a dose-dependent reduction of brachial and central BP. The hemodynamic effect was not mediated by the renin-angiotensin-aldosterone system. NaNO infusion resulted in a vasopressin-independent decrease in C and urine output but no change in urinary sodium excretion or GFR. The lack of increase in cGMP accompanying the increase in [Formula: see text] suggests a direct effect of nitrite or nitrate on the renal tubules and vascular bed with little or no systemic conversion to NO.
[Mh] Termos MeSH primário: Pressão Arterial/efeitos dos fármacos
Artéria Braquial/efeitos dos fármacos
Taxa de Filtração Glomerular/efeitos dos fármacos
Rim/efeitos dos fármacos
Natriurese/efeitos dos fármacos
Natriuréticos/administração & dosagem
Doadores de Óxido Nítrico/administração & dosagem
Nitrito de Sódio/administração & dosagem
Micção/efeitos dos fármacos
Vasodilatadores/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Aquaporina 2/metabolismo
Biomarcadores/sangue
Estudos Cross-Over
GMP Cíclico/metabolismo
Relação Dose-Resposta a Droga
Canais Epiteliais de Sódio/metabolismo
Feminino
Voluntários Saudáveis
Seres Humanos
Rim/metabolismo
Masculino
Natriuréticos/metabolismo
Nitratos/metabolismo
Óxido Nítrico/metabolismo
Doadores de Óxido Nítrico/metabolismo
Nitritos/metabolismo
Sistema Renina-Angiotensina/efeitos dos fármacos
Método Simples-Cego
Nitrito de Sódio/metabolismo
Fatores de Tempo
Urodinâmica/efeitos dos fármacos
Vasodilatadores/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (AQP2 protein, human); 0 (Aquaporin 2); 0 (Biomarkers); 0 (Epithelial Sodium Channels); 0 (Natriuretic Agents); 0 (Nitrates); 0 (Nitric Oxide Donors); 0 (Nitrites); 0 (SCNN1G protein, human); 0 (Vasodilator Agents); 31C4KY9ESH (Nitric Oxide); H2D2X058MU (Cyclic GMP); M0KG633D4F (Sodium Nitrite)
[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:170512
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00400.2016


  9 / 8516 MEDLINE  
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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


  10 / 8516 MEDLINE  
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[PMID]:28330966
[Au] Autor:Irsik DL; Blazer-Yost BL; Staruschenko A; Brands MW
[Ad] Endereço:Department of Physiology, Medical College of Georgia, Augusta, Georgia.
[Ti] Título:The normal increase in insulin after a meal may be required to prevent postprandial renal sodium and volume losses.
[So] Source:Am J Physiol Regul Integr Comp Physiol;312(6):R965-R972, 2017 Jun 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite the effects of insulinopenia in type 1 diabetes and evidence that insulin stimulates multiple renal sodium transporters, it is not known whether normal variation in plasma insulin regulates sodium homeostasis physiologically. This study tested whether the normal postprandial increase in plasma insulin significantly attenuates renal sodium and volume losses. Rats were instrumented with chronic artery and vein catheters, housed in metabolic cages, and connected to hydraulic swivels. Measurements of urine volume and sodium excretion (UNaV) over 24 h and the 4-h postprandial period were made in control (C) rats and insulin-clamped (IC) rats in which the postprandial increase in insulin was prevented. Twenty-four-hour urine volume (36 ± 3 vs. 15 ± 2 ml/day) and UNaV (3.0 ± 0.2 vs. 2.5 ± 0.2 mmol/day) were greater in the IC compared with C rats, respectively. Four hours after rats were given a gel meal, blood glucose and urine volume were greater in IC rats, but UNaV decreased. To simulate a meal while controlling blood glucose, C and IC rats received a glucose bolus that yielded peak increases in blood glucose that were not different between groups. Urine volume (9.7 ± 0.7 vs. 6.0 ± 0.8 ml/4 h) and UNaV (0.50 ± 0.08 vs. 0.20 ± 0.06 mmol/4 h) were greater in the IC vs. C rats, respectively, over the 4-h test. These data demonstrate that the normal increase in circulating insulin in response to hyperglycemia may be required to prevent excessive renal sodium and volume losses and suggest that insulin may be a physiological regulator of sodium balance.
[Mh] Termos MeSH primário: Hiperglicemia/sangue
Insulina/sangue
Rim/metabolismo
Natriurese
Período Pós-Prandial
Eliminação Renal
Sódio/urina
Micção
[Mh] Termos MeSH secundário: Animais
Biomarcadores/sangue
Glicemia/metabolismo
Técnica Clamp de Glucose
Hiperglicemia/fisiopatologia
Hiperglicemia/urina
Masculino
Modelos Animais
Ratos Sprague-Dawley
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Blood Glucose); 0 (Insulin); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00354.2016



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