Base de dados : MEDLINE
Pesquisa : D27.505.519.562.750.374 [Categoria DeCS]
Referências encontradas : 169 [refinar]
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  1 / 169 MEDLINE  
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[PMID]:28481660
[Au] Autor:Scott DW; Walker MP; Sesma J; Wu B; Stuhlmiller TJ; Sabater JR; Abraham WM; Crowder TM; Christensen DJ; Tarran R
[Ad] Endereço:1 Spyryx Biosciences, Durham, North Carolina.
[Ti] Título:SPX-101 Is a Novel Epithelial Sodium Channel-targeted Therapeutic for Cystic Fibrosis That Restores Mucus Transport.
[So] Source:Am J Respir Crit Care Med;196(6):734-744, 2017 Sep 15.
[Is] ISSN:1535-4970
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Cystic fibrosis (CF) lung disease is caused by the loss of function of the cystic fibrosis transmembrane conductance regulator (CFTR) combined with hyperactivation of the epithelial sodium channel (ENaC). In the lung, ENaC is responsible for movement of sodium. Hyperactivation of ENaC, which creates an osmotic gradient that pulls fluid out of the airway, contributes to reduced airway hydration, causing mucus dehydration, decreased mucociliary clearance, and recurrent acute bacterial infections. ENaC represents a therapeutic target to treat all patients with CF independent of their underlying CFTR mutation. OBJECTIVES: To investigate the in vitro and in vivo efficacy of SPX-101, a peptide mimetic of the natural regulation of ENaC activity by short palate, lung, and nasal epithelial clone 1, known as SPLUNC1. METHODS: ENaC internalization by SPX-101 in primary human bronchial epithelial cells from healthy and CF donors was assessed by surface biotinylation and subsequent Western blot analysis. SPX-101's in vivo therapeutic effect was assessed by survival of ß-ENaC-transgenic mice, mucus transport in these mice, and mucus transport in a sheep model of CF. MEASUREMENTS AND MAIN RESULTS: SPX-101 binds selectively to ENaC and promotes internalization of the α-, ß-, and γ-subunits. Removing ENaC from the membrane with SPX-101 causes a significant decrease in amiloride-sensitive current. The peptide increases survival of ß-ENaC-transgenic mice to greater than 90% with once-daily dosing by inhalation. SPX-101 increased mucus transport in the ß-ENaC mouse model as well as the sheep model of CF. CONCLUSIONS: These data demonstrate that SPX-101 promotes durable reduction of ENaC membrane concentration, leading to significant improvements in mucus transport.
[Mh] Termos MeSH primário: Regulador de Condutância Transmembrana em Fibrose Cística/uso terapêutico
Fibrose Cística/tratamento farmacológico
Bloqueadores do Canal de Sódio Epitelial/uso terapêutico
Canais Epiteliais de Sódio/uso terapêutico
Depuração Mucociliar/efeitos dos fármacos
Mucosa Respiratória/efeitos dos fármacos
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epithelial Sodium Channel Blockers); 0 (Epithelial Sodium Channels); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE
[do] DOI:10.1164/rccm.201612-2445OC


  2 / 169 MEDLINE  
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[PMID]:28334404
[Au] Autor:Bigiani A
[Ad] Endereço:Dipartimento di Scienze Biomediche, Metaboliche e Neuroscienze, Università di Modena e Reggio Emilia, Via G. Campi 287, 41125 Modena, Italy.
[Ti] Título:Calcium Homeostasis Modulator 1-Like Currents in Rat Fungiform Taste Cells Expressing Amiloride-Sensitive Sodium Currents.
[So] Source:Chem Senses;42(4):343-359, 2017 May 01.
[Is] ISSN:1464-3553
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Salt reception by taste cells is still the less understood transduction process occurring in taste buds, the peripheral sensory organs for the detection of food chemicals. Although there is evidence suggesting that the epithelial sodium channel (ENaC) works as sodium receptor, yet it is not clear how salt-detecting cells signal the relevant information to nerve endings. Taste cells responding to sweet, bitter, and umami substances release ATP as neurotransmitter through a nonvesicular mechanism. Three different channel proteins have been proposed as conduit for ATP secretion: pannexin channels, connexin hemichannels, and calcium homeostasis modulator 1 (CALHM1) channels. In heterologous expression systems, these channels mediate outwardly rectifying membrane currents with distinct biophysical and pharmacological properties. I therefore tested whether also salt-detecting taste cells were endowed with these currents. To this aim, I applied the patch-clamp techniques to single cells in isolated taste buds from rat fungiform papillae. Salt-detecting cells were functionally identified by exploiting the effect of amiloride, which induces a current response by shutting down ENaCs. I looked for the presence of outwardly rectifying currents by using appropriate voltage-clamp protocols and specific pharmacological tools. I found that indeed salt-detecting cells possessed these currents with properties consistent with the presence, at least in part, of CALHM1 channels. Unexpectedly, CALHM1-like currents in taste cells were potentiated by known blockers of pannexin, suggesting a possible inhibitory action of this protein on CALMH1. These findings indicate that communication between salt-detecting cells and nerve endings might involve ATP release by CALMH1 channels.
[Mh] Termos MeSH primário: Canais de Cálcio/fisiologia
Papilas Gustativas/citologia
Paladar/fisiologia
[Mh] Termos MeSH secundário: Amilorida/farmacologia
Animais
Bloqueadores do Canal de Sódio Epitelial
Homeostase
Técnicas de Patch-Clamp
Ratos
Canais de Sódio/efeitos dos fármacos
Cloreto de Sódio
Papilas Gustativas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CALHM1 protein, rat); 0 (Calcium Channels); 0 (Epithelial Sodium Channel Blockers); 0 (Sodium Channels); 451W47IQ8X (Sodium Chloride); 7DZO8EB0Z3 (Amiloride)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1093/chemse/bjx013


  3 / 169 MEDLINE  
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[PMID]:28152000
[Au] Autor:Tang L; Fang X; Winesett SP; Cheng CY; Binder HJ; Rivkees SA; Cheng SX
[Ad] Endereço:Department of Pediatrics, University of Florida, Gainesville, FL, United States of America.
[Ti] Título:Bumetanide increases Cl--dependent short-circuit current in late distal colon: Evidence for the presence of active electrogenic Cl- absorption.
[So] Source:PLoS One;12(2):e0171045, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mammalian colonic epithelia consist of cells that are capable of both absorbing and secreting Cl-. The present studies employing Ussing chamber technique identified two opposing short-circuit current (Isc) responses to basolateral bumetanide in rat distal colon. Apart from the transepithelial Cl--secretory Isc in early distal colon that was inhibited by bumetanide, bumetanide also stimulated Isc in late distal colon that had not previously been identified. Since bumetanide inhibits basolateral Na+-K+-2Cl- cotransporter (NKCC) in crypt cells and basolateral K+-Cl- cotransporter (KCC) in surface epithelium, we proposed this stimulatory Isc could represent a KCC-mediated Cl- absorptive current. In support of this hypothesis, ion substitution experiments established Cl- dependency of this absorptive Isc and transport inhibitor studies demonstrated the involvement of an apical Cl- conductance. Current distribution and RNA sequencing analyses revealed that this Cl- absorptive Isc is closely associated with epithelial Na+ channel (ENaC) but is not dependent on ENaC activity. Thus, inhibition of ENaC by 10 µM amiloride or benzamil neither altered the direction nor its activity. Physiological studies suggested that this Cl- absorptive Isc senses dietary Cl- content; thus when dietary Cl- was low, Cl- absorptive Isc was up-regulated. In contrast, when dietary Cl- was increased, Cl- absorptive Isc was down-regulated. We conclude that an active Cl- extrusion mechanism exists in ENaC-expressing late distal colon and likely operates in parallel with ENaC to facilitate NaCl absorption.
[Mh] Termos MeSH primário: Bumetanida/farmacologia
Cloretos/metabolismo
Colo/efeitos dos fármacos
Colo/metabolismo
[Mh] Termos MeSH secundário: Amilorida/análogos & derivados
Amilorida/farmacologia
Animais
Bário/farmacologia
Cloretos/farmacologia
Bloqueadores do Canal de Sódio Epitelial/farmacologia
Canais Epiteliais de Sódio/genética
Canais Epiteliais de Sódio/metabolismo
Epitélio/efeitos dos fármacos
Epitélio/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Glibureto/farmacologia
Masculino
Técnicas de Cultura de Órgãos
Ratos Sprague-Dawley
Sódio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chlorides); 0 (Epithelial Sodium Channel Blockers); 0 (Epithelial Sodium Channels); 04659UUJ94 (benzamil); 0Y2S3XUQ5H (Bumetanide); 24GP945V5T (Barium); 7DZO8EB0Z3 (Amiloride); 9NEZ333N27 (Sodium); SX6K58TVWC (Glyburide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170203
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0171045


  4 / 169 MEDLINE  
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[PMID]:28107195
[Au] Autor:Zhu BY; Shang BY; Du Y; Li Y; Li L; Xu XD; Zhen YS
[Ad] Endereço:Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.
[Ti] Título:A new HDAC inhibitor cinnamoylphenazine shows antitumor activity in association with intensive macropinocytosis.
[So] Source:Oncotarget;8(9):14748-14758, 2017 Feb 28.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies have shown that intensive macropinocytosis occurs in cancer cells and neutral red (NR) is noted for its capability to enter into the cell massively through a process mimetic to macropinocytosis. In addition, trans-cinnamic acid (tCA) has been found to be an inhibitor of histone deacetylase (HDAC). In the present study, cinnamoylphenazine (CA-PZ) that consists of NR and tCA moieties was synthesized and evaluated. As shown, CA-PZ massively entered into colon carcinoma HT-29 cells and pancreatic carcinoma MIA PaCa-2 cells and this entry was blocked by 5-(N-ethyl-N-isopropyl) amiloride (EIPA, an inhibitor of macropinocytosis), indicating a macropinocytosis-mediated uptake. Furthermore, CA-PZ markedly increased the protein expression levels of acetyl-H3, acetyl-H4 and p21 in HT-29 cells and MIA PaCa-2 cells. CA-PZ significantly inhibited the growth of colon carcinoma HT-29 and pancreatic carcinoma MIA PaCa-2 xenografts. By in vivo imaging, CA-PZ displayed prominent accumulation in the tumor xenografts. The study indicates that the newly synthesized CA-PZ acts as an HDAC inhibitor in association with intensive macropinocytosis-mediated intracellular delivery in cancer cells. The use of neutral red for preparation of chimeric molecules with the attribute of macropinocytosis-mediated intracellular delivery might open an alternative way for development of HDAC inhibitors.
[Mh] Termos MeSH primário: Cinamatos/farmacologia
Neoplasias do Colo/tratamento farmacológico
Inibidores de Histona Desacetilases/farmacologia
Neoplasias Pancreáticas/tratamento farmacológico
Fenazinas/farmacologia
Pinocitose/efeitos dos fármacos
Ensaios Antitumorais Modelo de Xenoenxerto
[Mh] Termos MeSH secundário: Células A549
Amilorida/análogos & derivados
Amilorida/farmacologia
Animais
Western Blotting
Linhagem Celular Tumoral
Cinamatos/síntese química
Neoplasias do Colo/metabolismo
Neoplasias do Colo/patologia
Bloqueadores do Canal de Sódio Epitelial/farmacologia
Feminino
Células HCT116
Células HT29
Inibidores de Histona Desacetilases/síntese química
Seres Humanos
Camundongos Endogâmicos BALB C
Camundongos Nus
Microscopia Confocal
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/patologia
Fenazinas/síntese química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cinnamates); 0 (Epithelial Sodium Channel Blockers); 0 (Histone Deacetylase Inhibitors); 0 (Phenazines); 0 (cinnamoylphenazine); 7DZO8EB0Z3 (Amiloride); VW50CE070T (ethylisopropylamiloride)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170121
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.14714


  5 / 169 MEDLINE  
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[PMID]:28082350
[Au] Autor:Bai J; Chow BK
[Ad] Endereço:School of Biological Sciences, University of Hong Kong, Hong Kong, China.
[Ti] Título:Secretin is involved in sodium conservation through the renin-angiotensin-aldosterone system.
[So] Source:FASEB J;31(4):1689-1697, 2017 Apr.
[Is] ISSN:1530-6860
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Secretin (SCT) and its receptor (SCTR) are important in fluid regulation at multiple levels the modulation of expression and translocation of renal aquaporin 2 and functions of central angiotensin II (ANGII). The functional interaction of SCT with peripheral ANGII, however, remains unknown. As the ANGII-aldosterone axis dominates the regulation of renal epithelial sodium channel (ENaC) function, we therefore tested whether SCT/SCTR can regulate sodium homeostasis the renin-angiotensin-aldosterone system. SCTR-knockout (SCTR ) mice showed impaired aldosterone synthase (CYP11B2) expression and, consequently, aldosterone release upon intraperitoneal injection of ANGII. Endogenous ANGII production induced by dietary sodium restriction was higher in SCTR than in C57BL/6N [wild-type (WT)] mice, but CYP11B2 and aldosterone synthesis were not elevated. Reduced accumulation of cholesteryl ester-the precursor of aldosterone-was observed in adrenal glands of SCTR mice that were fed a low-sodium diet. Absence of SCTR resulted in elevated basal transcript levels of adrenal CYP11B2 and renal ENaCs. Although transcript and protein levels of ENaCs were similar in WT and SCTR mice under sodium restriction, ENaCs in SCTR mice were less sensitive to amiloride hydrochloride. In summary, the SCT/SCTR axis is involved in aldosterone precursor uptake, and the knockout of SCTR results in defective aldosterone biosynthesis/release and altered sensitivity of ENaCs to amiloride.-Bai, J., Chow, B. K. C. Secretin is involved in sodium conservation through the renin-angiotensin-aldosterone system.
[Mh] Termos MeSH primário: Aldosterona/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
Receptores dos Hormônios Gastrointestinais/metabolismo
Sistema Renina-Angiotensina
Secretina/metabolismo
Sódio na Dieta/metabolismo
[Mh] Termos MeSH secundário: Glândulas Suprarrenais/metabolismo
Amilorida/farmacologia
Angiotensina II/metabolismo
Animais
Citocromo P-450 CYP11B2/genética
Citocromo P-450 CYP11B2/metabolismo
Bloqueadores do Canal de Sódio Epitelial/farmacologia
Canais Epiteliais de Sódio/metabolismo
Rim/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Receptores Acoplados a Proteínas-G/genética
Receptores dos Hormônios Gastrointestinais/genética
Sódio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epithelial Sodium Channel Blockers); 0 (Epithelial Sodium Channels); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Gastrointestinal Hormone); 0 (Sodium, Dietary); 0 (secretin receptor); 11128-99-7 (Angiotensin II); 1393-25-5 (Secretin); 4964P6T9RB (Aldosterone); 7DZO8EB0Z3 (Amiloride); 9NEZ333N27 (Sodium); EC 1.14.15.4 (Cytochrome P-450 CYP11B2)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.1096/fj.201600911R


  6 / 169 MEDLINE  
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[PMID]:27989677
[Au] Autor:Pontes G; Pereira MH; Barrozo RB
[Ad] Endereço:Grupo de Neuroetología de Insectos Vectores, Laboratorio Fisiología de Insectos, IBBEA, CONICET-UBA, DBBE, Facultad Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, BA, Argentina.
[Ti] Título:Salt controls feeding decisions in a blood-sucking insect.
[So] Source:J Insect Physiol;98:93-100, 2017 Apr.
[Is] ISSN:1879-1611
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Salts are necessary for maintaining homeostatic conditions within the body of all living organisms. Like with all essential nutrients, deficient or excessive ingestion of salts can result in adverse health effects. The taste system is a primary sensory modality that helps animals to make adequate feeding decisions in terms of salt consumption. In this work we show that sodium and potassium chloride salts modulate the feeding behavior of Rhodnius prolixus in a concentration-dependent manner. Feeding is only triggered by an optimal concentration of any of these salts (0.1-0.15M) and in presence of the phagostimulant ATP. Conversely, feeding solutions that do not contain salts or have a high-salt concentration (>0.3M) are not ingested by insects. Notably, we show that feeding decisions of insects cannot be explained as an osmotic effect, because they still feed over hyperosmotic solutions bearing the optimal salt concentration. Insects perceive optimal-salt, no-salt and high-salt solutions as different gustatory information, as revealed the electromyogram recordings of the cibarial pump. Moreover, because insects do a continuous gustatory monitoring of the incoming food during feeding, sudden changes beyond the optimal sodium concentration decrease and even inhibit feeding. The administration of amiloride, a sodium channel blocker, noticeably reduces the ingestion of the optimal sodium solution but not of the optimal potassium solution. Salt detection seems to occur at least through two salt receptors, one amiloride-sensitive and another amiloride-insensitive. Our results confirm the importance of the gustatory system in R. prolixus, showing the relevant role that salts play on their feeding decisions.
[Mh] Termos MeSH primário: Amilorida/farmacologia
Bloqueadores do Canal de Sódio Epitelial/farmacologia
Rhodnius/fisiologia
Cloreto de Sódio/farmacologia
Percepção Gustatória
[Mh] Termos MeSH secundário: Animais
Comportamento Alimentar/efeitos dos fármacos
Ninfa/efeitos dos fármacos
Ninfa/fisiologia
Rhodnius/efeitos dos fármacos
Rhodnius/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epithelial Sodium Channel Blockers); 451W47IQ8X (Sodium Chloride); 7DZO8EB0Z3 (Amiloride)
[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:161220
[St] Status:MEDLINE


  7 / 169 MEDLINE  
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[PMID]:28082810
[Au] Autor:Yang C; Xiong Y; Zhang SS; An FM; Sun J; Zhang QL; Zhan Q
[Ad] Endereço:Cheng Yang, Fang-Mei An, Jing Sun, Qing-Lin Zhang, Qiang Zhan, Department of Gastroenterology, Wuxi People's Hospital, Nanjing Medical University, Wuxi 214023, Jiangsu Province, China.
[Ti] Título:Regulating effect of TongXie-YaoFang on colonic epithelial secretion Cl and HCO channel.
[So] Source:World J Gastroenterol;22(48):10584-10591, 2016 Dec 28.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: To investigate the pharmacological effect of TongXie-YaoFang (TXYF) formula, a Chinese herbal formula, on Diarrhea-predominant irritable bowel syndrome (D-IBS) rats. METHODS: In a neonatal maternal separation plus restraint stress (NMS + RS) model of D-IBS, male Sprague Dawley rats were randomly divided into two groups (NMS + RS group and TXYF-formula group) with no handlings were used as controls (NH group). Starting from postnatal day 60, rats in TXYF-formula group were administered TXYF-formula (4.92 g/100 g bodyweight) orally twice a day for 14 consecutive days while NH group and NMS + RS group were given distilled water. Using short-circuit current technology, we observed 5-HT-induced changes of current across ion channels, such as cystic fibrosis transmembrane conductance regulator (CFTR) Cl channel, epithelial Na channel (ENaC), Ca -dependent Cl channel (CACC), Na -K -2Cl co-transporter (NKCC), and Na -HCO co-transporter (NBC), in the colonic epithelium of three groups after exposure to drugs and specific blockers with a Power Lab System (AD Instruments International). RESULTS: Under basal conditions, the changes of short-circuit current (∆Isc, µA/cm ) induced by 5-HT were similar in NH group and TXYF-formula group, and both higher than NMS + RS group (70.86 µA/cm ± 12.32 µA/cm , 67.67 µA/cm ± 11.68 µA/cm 38.8 µA/cm ± 7.25 µA/cm , < 0.01, respectively). When CACC was blocked by 4,4'-diisothiocyanato-stilbene-2,2'-disulfonic acid, 5-HT-induced ∆Isc was smaller in NMS + RS group than in NH group and TXYF-formula group, respectively (48.41 µA/cm ± 13.15 µA/cm 74.62 µA/cm ± 10.73 µA/cm , 69.22 µA/cm ± 11.7 µA/cm , < 0.05, respectively). The similar result could be obtained when ENaC was blocked by Amiloride (44.69 µA/cm ± 12.58 µA/cm 62.05 µA/cm ± 11.26 µA/cm , 62.11 µA/cm ± 12.01 µA/cm , < 0.05, respectively). However, when CFTR Cl channel was blocked by 1,1-dimethyl piperidinium chloride (DPC), 5-HT-induced ∆Isc did not significantly differ in three groups (42.28 µA/cm ± 10.61 µA/cm 51.48 µA/cm ± 6.56 µA/cm 47.75 µA/cm ± 7.99 µA/cm , > 0.05, respectively). The similar results could also be obtained in three groups when NBC and NKCC were respectively blocked by their blockers. CONCLUSION: TXYF-formula can regulate the Cl and HCO secretion of colonic mucosa CFTR Cl channel, Cl /HCO exchanger, NBC and NKCC co-transporters.
[Mh] Termos MeSH primário: Canais de Cloreto/efeitos dos fármacos
Diarreia/metabolismo
Medicamentos de Ervas Chinesas/farmacologia
Mucosa Intestinal/efeitos dos fármacos
Síndrome do Intestino Irritável/metabolismo
Simportadores de Sódio-Bicarbonato/efeitos dos fármacos
[Mh] Termos MeSH secundário: 5-Hidroxitriptofano/farmacologia
Adulto
Amilorida/farmacologia
Animais
Canais de Cloreto/antagonistas & inibidores
Colo/metabolismo
Colo/secreção
Diarreia/tratamento farmacológico
Diarreia/etiologia
Bloqueadores do Canal de Sódio Epitelial/farmacologia
Seres Humanos
Mucosa Intestinal/secreção
Síndrome do Intestino Irritável/tratamento farmacológico
Síndrome do Intestino Irritável/etiologia
Masculino
Privação Materna
Piperidinas/farmacologia
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Inibidores de Simportadores de Cloreto de Sódio e Potássio/farmacologia
Simportadores de Sódio-Bicarbonato/antagonistas & inibidores
Simportadores de Cloreto de Sódio-Potássio/efeitos dos fármacos
Estresse Psicológico/complicações
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chloride Channels); 0 (Drugs, Chinese Herbal); 0 (Epithelial Sodium Channel Blockers); 0 (Piperidines); 0 (Sodium Potassium Chloride Symporter Inhibitors); 0 (Sodium-Bicarbonate Symporters); 0 (Sodium-Potassium-Chloride Symporters); 0 (tongxie-yaofang); 7DZO8EB0Z3 (Amiloride); C1LJO185Q9 (5-Hydroxytryptophan); S2SFZ0Z4TW (mepiquat)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.3748/wjg.v22.i48.10584


  8 / 169 MEDLINE  
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[PMID]:27707706
[Au] Autor:Layton AT; Laghmani K; Vallon V; Edwards A
[Ad] Endereço:Department of Mathematics, Duke University, Durham, North Carolina; alayton@math.duke.edu.
[Ti] Título:Solute transport and oxygen consumption along the nephrons: effects of Na+ transport inhibitors.
[So] Source:Am J Physiol Renal Physiol;311(6):F1217-F1229, 2016 Dec 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sodium and its associated anions are the major determinant of extracellular fluid volume, and the reabsorption of Na by the kidney plays a crucial role in long-term blood pressure control. The goal of this study was to investigate the extent to which inhibitors of transepithelial Na transport (T ) along the nephron alter urinary solute excretion and T efficiency and how those effects may vary along different nephron segments. To accomplish that goal, we used the multinephron model developed in the companion study (28). That model represents detailed transcellular and paracellular transport processes along the nephrons of a rat kidney. We simulated the inhibition of the Na /H exchanger (NHE3), the bumetanide-sensitive Na -K -2Cl transporter (NKCC2), the Na -Cl cotransporter (NCC), and the amiloride-sensitive Na channel (ENaC). Under baseline conditions, NHE3, NKCC2, NCC, and ENaC reabsorb 36, 22, 4, and 7%, respectively, of filtered Na The model predicted that inhibition of NHE3 substantially reduced proximal tubule T and oxygen consumption (Q ). Whole-kidney T efficiency, as reflected by the number of moles of Na reabsorbed per moles of O consumed (denoted by the ratio T /Q ), decreased by ∼20% with 80% inhibition of NHE3. NKCC2 inhibition simulations predicted a substantial reduction in thick ascending limb T and Q ; however, the effect on whole-kidney T /Q was minor. Tubular K transport was also substantially impaired, resulting in elevated urinary K excretion. The most notable effect of NCC inhibition was to increase the excretion of Na , K , and Cl ; its impact on whole-kidney T and its efficiency was minor. Inhibition of ENaC was predicted to have opposite effects on the excretion of Na (increased) and K (decreased) and to have only a minor impact on whole-kidney T and T /Q Overall, model predictions agree well with measured changes in Na and K excretion in response to diuretics and Na transporter mutations.
[Mh] Termos MeSH primário: Bloqueadores do Canal de Sódio Epitelial/farmacologia
Modelos Biológicos
Néfrons/efeitos dos fármacos
Consumo de Oxigênio/efeitos dos fármacos
Trocadores de Sódio-Hidrogênio/antagonistas & inibidores
Membro 1 da Família 12 de Carreador de Soluto/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Transporte de Íons/efeitos dos fármacos
Néfrons/metabolismo
Ratos
Trocador 3 de Sódio-Hidrogênio
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epithelial Sodium Channel Blockers); 0 (Slc9a3 protein, rat); 0 (Sodium-Hydrogen Exchanger 3); 0 (Sodium-Hydrogen Exchangers); 0 (Solute Carrier Family 12, Member 1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161007
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00294.2016


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[PMID]:27592201
[Au] Autor:Galiana-Simal A; Olivares-Álvaro E; Klett-Mingo M; Ruiz-Roso MB; Ballesteros S; de Las Heras N; Fuller PJ; Lahera V; Martín-Fernández B
[Ad] Endereço:Department of Physiology, Faculty of Medicine, Universidad Complutense, 28040 Madrid, Spain.
[Ti] Título:Proanthocyanidins block aldosterone-dependent up-regulation of cardiac gamma ENaC and Nedd4-2 inactivation via SGK1.
[So] Source:J Nutr Biochem;37:13-19, 2016 11.
[Is] ISSN:1873-4847
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aldosterone plays a central role in the development of cardiac pathological states involving ion transport imbalances, especially sodium transport. We have previously demonstrated a cardioprotective effect of proanthocyanidins in aldosterone-treated rats. Our objective was to investigate for the first time the effect of proanthocyanidins on serum and glucocorticoid-regulated kinase 1 (SGK1), epithelial Na channel (γ-ENaC), neuronal precursor cells expressed developmentally down-regulated 4-2 (Nedd4-2) and phosphoNedd4-2 protein expression in the hearts of aldosterone-treated rats. Male Wistar rats received aldosterone (1mg kg day )+1% NaCl for 3weeks. Half of the animals in each group were simultaneously treated with the proanthocyanidins-rich extract (80% w/w) (PRO80, 5mg kg day ). Hypertension and diastolic dysfunction induced by aldosterone were abolished by treatment with PRO80. Expression of fibrotic, inflammatory and oxidative mediators were increased by aldosterone-salt administration and blunted by PRO80. Antioxidant capacity was improved by PRO80. The up-regulated aldosterone mediator SGK1, ENaC and p-Nedd4-2/total Nedd4-2 ratio were blocked by PRO80. PRO80 blunted aldosterone-mineralocorticoid-mediated up-regulation of ENaC provides new mechanistic insight of the beneficial effect of proanthocyanidins preventing the cardiac alterations induced by aldosterone excess.
[Mh] Termos MeSH primário: Suplementos Nutricionais
Complexos Endossomais de Distribuição Requeridos para Transporte/antagonistas & inibidores
Canais Epiteliais de Sódio/metabolismo
Ventrículos do Coração/metabolismo
Proteínas Imediatamente Precoces/antagonistas & inibidores
Proantocianidinas/uso terapêutico
Proteínas Serina-Treonina Quinases/antagonistas & inibidores
Ubiquitina-Proteína Ligases/antagonistas & inibidores
Disfunção Ventricular Esquerda/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/uso terapêutico
Anti-Hipertensivos/uso terapêutico
Antioxidantes/uso terapêutico
Biomarcadores/metabolismo
Cardiomegalia/etiologia
Cardiomegalia/prevenção & controle
Cardiotônicos/uso terapêutico
Complexos Endossomais de Distribuição Requeridos para Transporte/agonistas
Complexos Endossomais de Distribuição Requeridos para Transporte/metabolismo
Agonistas do Canal de Sódio Epitelial/antagonistas & inibidores
Agonistas do Canal de Sódio Epitelial/metabolismo
Bloqueadores do Canal de Sódio Epitelial/uso terapêutico
Canais Epiteliais de Sódio/química
Fibrose
Ventrículos do Coração/imunologia
Ventrículos do Coração/patologia
Ventrículos do Coração/fisiopatologia
Hipertensão/etiologia
Hipertensão/prevenção & controle
Proteínas Imediatamente Precoces/agonistas
Proteínas Imediatamente Precoces/metabolismo
Masculino
Antagonistas de Receptores de Mineralocorticoides/uso terapêutico
Ubiquitina-Proteína Ligases Nedd4
Estresse Oxidativo
Proteínas Serina-Treonina Quinases/metabolismo
Ratos Wistar
Ubiquitina-Proteína Ligases/metabolismo
Disfunção Ventricular Esquerda/metabolismo
Disfunção Ventricular Esquerda/patologia
Disfunção Ventricular Esquerda/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antihypertensive Agents); 0 (Antioxidants); 0 (Biomarkers); 0 (Cardiotonic Agents); 0 (Endosomal Sorting Complexes Required for Transport); 0 (Epithelial Sodium Channel Agonists); 0 (Epithelial Sodium Channel Blockers); 0 (Epithelial Sodium Channels); 0 (Immediate-Early Proteins); 0 (Mineralocorticoid Receptor Antagonists); 0 (Proanthocyanidins); EC 2.3.2.26 (NEDD4L protein, rat); EC 2.3.2.26 (Nedd4 Ubiquitin Protein Ligases); EC 2.3.2.26 (Nedd4 protein, rat); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (serum-glucocorticoid regulated kinase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160905
[St] Status:MEDLINE


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[PMID]:27214087
[Au] Autor:Andersen H; Hansen PB; Bistrup C; Nielsen F; Henriksen JE; Jensen BL
[Ad] Endereço:aDepartment of Cardiovascular and Renal Research, Institute of Molecular Medicine, University of Southern Denmark bDepartment of Nephrology, Odense University Hospital cClinical Pharmacology, Institute of Public Health, University of Southern Denmark dDepartment of Endocrinology, Odense University Hospital, Odense, Denmark.
[Ti] Título:Significant natriuretic and antihypertensive action of the epithelial sodium channel blocker amiloride in diabetic patients with and without nephropathy.
[So] Source:J Hypertens;34(8):1621-9, 2016 Aug.
[Is] ISSN:1473-5598
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Diabetic nephropathy is associated with aberrant glomerular filtration of serine proteases. The study was designed to test the hypothesis that the epithelial sodium channel is activated proteolytically by urine plasmin in diabetic nephropathy and mediates renal sodium retention. METHODS: In an open-label intervention study on type 1 diabetes patients on standardized NaCl intake (200 mmol/day) with (n = 15) and without diabetic nephropathy (control, n = 12), urinary Na excretion in response to oral amiloride (20 or 40 mg/day for 2 days) was compared. RESULTS: A total of 27 patients completed the study and nine diabetic nephropathy and eight control study participants were compliant (24-h urine Na excretion of 200 mmol ±â€Š30%). Amiloride increased significantly total and fractional Na excretion in both groups. Total natriuresis and weight loss were significantly larger in the control group compared with diabetic nephropathy at day 1 of amiloride, whereas fractional Na excretion did not differ. Amiloride intervention increased plasma renin concentration only in diabetic nephropathy group; it reduced SBP in both groups, whereas DBP was reduced in diabetic nephropathy group only. Albuminuria was reduced significantly by amiloride in diabetic nephropathy group. Urine total amiloride concentration was not different between groups (12 ±â€Š1 and 16 ±â€Š1 µmol/l, respectively). Urine total plasminogen and active plasmin were reduced after amiloride in diabetic nephropathy. CONCLUSION: Amiloride increased renal Na excretion, reduced blood pressure, albuminuria, and total and active plasmin in urine. It is concluded that epithelial sodium channel is an attractive target to attain blood pressure control in long-term type I diabetes with no enhanced activity associated with nephropathy.
[Mh] Termos MeSH primário: Amilorida/farmacologia
Diabetes Mellitus Tipo 1/fisiopatologia
Nefropatias Diabéticas/fisiopatologia
Bloqueadores do Canal de Sódio Epitelial/farmacologia
Natriurese/efeitos dos fármacos
Sódio/urina
[Mh] Termos MeSH secundário: Albuminúria/tratamento farmacológico
Amilorida/uso terapêutico
Amilorida/urina
Pressão Sanguínea/efeitos dos fármacos
Diabetes Mellitus Tipo 1/complicações
Nefropatias Diabéticas/sangue
Nefropatias Diabéticas/etiologia
Nefropatias Diabéticas/urina
Bloqueadores do Canal de Sódio Epitelial/uso terapêutico
Bloqueadores do Canal de Sódio Epitelial/urina
Canais Epiteliais de Sódio
Feminino
Fibrinolisina/urina
Seres Humanos
Rim/fisiopatologia
Masculino
Meia-Idade
Plasminogênio/urina
Renina/sangue
Sódio na Dieta/administração & dosagem
Perda de Peso
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Epithelial Sodium Channel Blockers); 0 (Epithelial Sodium Channels); 0 (Sodium, Dietary); 7DZO8EB0Z3 (Amiloride); 9001-91-6 (Plasminogen); 9NEZ333N27 (Sodium); EC 3.4.21.7 (Fibrinolysin); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160524
[St] Status:MEDLINE
[do] DOI:10.1097/HJH.0000000000000967



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