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Pesquisa : D12.776.157.530.400.600.150 [Categoria DeCS]
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[PMID]:29235789
[Au] Autor:Danylovych YV; Chunikhin AY; Danylovych GV; Kolomiets OV
[Ti] Título:The use of the Petri net method in the simulation modeling of mitochondrial swelling.
[So] Source:Ukr Biochem J;88(4):66-74, 2016 Jul-Aug.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Using photon correlation spectroscopy, which allows investigating changes in the hydrodynamic dia­meter of the particles in suspension, it was shown that ultrahigh concentrations of Ca2+ (over 10 mM) induce swelling of isolated mitochondria. An increase in hydrodynamic diameter was caused by an increase of non-specific mitochondrial membrane permeability to Ca ions, matrix Ca2+ overload, activation of ATP- and Ca2+-sensitive K+-channels, as well as activation of cyclosporin-sensitive permeability transition pore. To formalize the experimental data and to assess conformity of experimental results with theoretical predictions we developed a simulation model using the hybrid functional Petri net method.
[Mh] Termos MeSH primário: Cálcio/farmacologia
Ciclosporina/farmacologia
Mitocôndrias/efeitos dos fármacos
Dilatação Mitocondrial/efeitos dos fármacos
Modelos Biológicos
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Cátions Bivalentes
Permeabilidade da Membrana Celular/efeitos dos fármacos
Simulação por Computador
Feminino
Transporte de Íons
Canais KATP/metabolismo
Cinética
Mitocôndrias/metabolismo
Proteínas de Transporte da Membrana Mitocondrial/metabolismo
Miométrio/química
Miométrio/metabolismo
Canais de Potássio Cálcio-Ativados/metabolismo
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cations, Divalent); 0 (KATP Channels); 0 (Mitochondrial Membrane Transport Proteins); 0 (Potassium Channels, Calcium-Activated); 0 (mitochondrial permeability transition pore); 83HN0GTJ6D (Cyclosporine); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171214
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.04.066


  2 / 2188 MEDLINE  
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[PMID]:28817716
[Au] Autor:Yin D; Wang Q; Zhou X; Li Y
[Ad] Endereço:Department of Nephrology, the Second Xiangya Hospital, Central South University, Key Laboratory of Kidney Disease and Blood Purification in Hunan, Changsha, China.
[Ti] Título:Endothelial dysfunction in renal arcuate arteries of obese Zucker rats: The roles of nitric oxide, endothelium-derived hyperpolarizing factors, and calcium-activated K+ channels.
[So] Source:PLoS One;12(8):e0183124, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The roles of nitric oxide (NO), endothelium-derived hyperpolarizing factors (EDHF), and calcium-activated K+ (KCa) channels in diabetes-associated endothelial dysfunction of small renal arteries are not clear. The present study investigated acetylcholine (ACh)-induced vasorelaxation of renal arcuate arteries from obese Zucker (OZ) rats at different diabetes durations, and the relative contribution of NO, EDHF, and KCa channels to the endothelial dysfunction. OZ rats of 7 weeks (prediabetic stage), 12 weeks (early diabetic stage), and 20 weeks (late diabetic stage), and time-matched lean control rats, were studied. Segments of arcuate arteries (130 to 180 µm) were isolated, cannulated and pressurized. Vascular endothelial functions were tested using ACh-induced vasodilation. Our experiments demonstrated: (1) ACh-elicited vasodilation was impaired in OZ rats of 20 weeks, but not in rats of 7 and 12 weeks; (2) inhibition of NO or EDHF (contributed by epoxyeicosatrienoic acids [EETs]) production significantly decreased ACh-induced vasodilation in both lean and OZ rats of 20 weeks. The reduction of ACh-induced vasodilation by inhibition of NO or EDHF formation was less in OZ rats, as compared to lean rats; and (3) inhibition of KCa channels markedly reduced ACh-induced vasodilation in lean control rats, but not in OZ rats of 20 weeks. Our observations indicated that endothelium-dependent vasodilation in renal arcuate arteries is impaired in diabetes mellitus; NO and EDHF, mainly EETs, dominate the ACh-induced vasodilation in renal arcuate arteries; the contribution of NO and EETs is impaired in diabetic rats; KCa channels are involved in ACh-induced vasodilation; and the activity of KCa channels is downregulated in diabetes mellitus.
[Mh] Termos MeSH primário: Artérias/fisiopatologia
Fatores Biológicos/fisiologia
Endotélio Vascular/fisiopatologia
Rim/irrigação sanguínea
Óxido Nítrico/fisiologia
Obesidade/fisiopatologia
Canais de Potássio Cálcio-Ativados/fisiologia
[Mh] Termos MeSH secundário: Animais
Estudos de Casos e Controles
Masculino
Ratos
Ratos Zucker
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biological Factors); 0 (Potassium Channels, Calcium-Activated); 0 (endothelium-dependent hyperpolarization factor); 31C4KY9ESH (Nitric Oxide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183124


  3 / 2188 MEDLINE  
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[PMID]:28512142
[Au] Autor:Zhu MX
[Ad] Endereço:Department of Integrative Biology and Pharmacology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030 michael.x.zhu@uth.tmc.edu.
[Ti] Título:A well-known potassium channel plays a critical role in lysosomes.
[So] Source:J Cell Biol;216(6):1513-1515, 2017 Jun 05.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Whole-endolysosome patch clamping presents new opportunities to identify and characterize channels pivotal for these acidic organelles. In this issue (Wang et al., 2017. https://doi.org/10.1083/jcb.201612123), the identification of a role for the large conductance calcium-activated potassium channel brings new thinking about regulation of lysosome membrane potential and function.
[Mh] Termos MeSH primário: Canais de Potássio Cálcio-Ativados
Canais de Potássio
[Mh] Termos MeSH secundário: Cálcio
Seres Humanos
Lisossomos
Potenciais da Membrana
Organelas
Técnicas de Patch-Clamp
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Potassium Channels); 0 (Potassium Channels, Calcium-Activated); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170518
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201704017


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[PMID]:28490422
[Au] Autor:Jantarajit W; Lertsuwan K; Teerapornpuntakit J; Krishnamra N; Charoenphandhu N
[Ad] Endereço:Center of Calcium and Bone Research, Faculty of Science, Mahidol University, Bangkok, Thailand.
[Ti] Título:CFTR-mediated anion secretion across intestinal epithelium-like Caco-2 monolayer under PTH stimulation is dependent on intermediate conductance K channels.
[So] Source:Am J Physiol Cell Physiol;313(1):C118-C129, 2017 Jul 01.
[Is] ISSN:1522-1563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Parathyroid hormone (PTH), a pleiotropic hormone that maintains mineral homeostasis, is also essential for controlling pH balance and ion transport across renal and intestinal epithelia. Optimization of luminal pH is important for absorption of trace elements, e.g., calcium and phosphorus. We have previously demonstrated that PTH rapidly stimulated electrogenic [Formula: see text] secretion in intestinal epithelial-like Caco-2 monolayers, but the underlying cellular mechanism, contributions of other ions, particularly Cl and K , and long-lasting responses are not completely understood. Herein, PTH and forskolin were confirmed to induce anion secretion, which peaked within 1-3 min (early phase), followed by an abrupt decay and plateau that lasted for 60 min (late phase). In both early and late phases, apical membrane capacitance was increased with a decrease in basolateral capacitance after PTH or forskolin exposure. PTH also induced a transient increase in apical conductance with a long-lasting decrease in basolateral conductance. Anion secretion in both phases was reduced under [Formula: see text]-free and/or Cl -free conditions or after exposure to carbonic anhydrase inhibitor (acetazolamide), CFTR inhibitor (CFTRinh-172), Na /H exchanger (NHE)-3 inhibitor (tenapanor), or K channel inhibitors (BaCl , clotrimazole, and TRAM-34; basolateral side), the latter of which suggested that PTH action was dependent on basolateral K recycling. Furthermore, early- and late-phase responses to PTH were diminished by inhibitors of PI3K (wortmannin and LY-294002) and PKA (PKI 14-22). In conclusion, PTH requires NHE3 and basolateral K channels to induce [Formula: see text] and Cl secretion, thus explaining how PTH regulated luminal pH balance and pH-dependent absorption of trace minerals.
[Mh] Termos MeSH primário: Regulador de Condutância Transmembrana em Fibrose Cística/metabolismo
Hormônio Paratireóideo/farmacologia
Fosfatidilinositol 3-Quinases/metabolismo
Canais de Potássio Cálcio-Ativados/metabolismo
ATPase Trocadora de Sódio-Potássio/metabolismo
[Mh] Termos MeSH secundário: Acetazolamida/farmacologia
Potenciais de Ação/efeitos dos fármacos
Androstadienos/farmacologia
Compostos de Bário/farmacologia
Bicarbonatos/metabolismo
Células CACO-2
Cálcio/metabolismo
Inibidores da Anidrase Carbônica/farmacologia
Cloretos/metabolismo
Cloretos/farmacologia
Cromonas/farmacologia
Clotrimazol/farmacologia
Colforsina/farmacologia
Regulador de Condutância Transmembrana em Fibrose Cística/antagonistas & inibidores
Regulador de Condutância Transmembrana em Fibrose Cística/genética
Condutividade Elétrica
Seres Humanos
Concentração de Íons de Hidrogênio
Transporte de Íons/efeitos dos fármacos
Isoquinolinas/farmacologia
Morfolinas/farmacologia
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/genética
Fósforo/metabolismo
Potássio/metabolismo
Canais de Potássio Cálcio-Ativados/antagonistas & inibidores
Canais de Potássio Cálcio-Ativados/genética
Pirazóis/farmacologia
ATPase Trocadora de Sódio-Potássio/antagonistas & inibidores
ATPase Trocadora de Sódio-Potássio/genética
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androstadienes); 0 (Barium Compounds); 0 (Bicarbonates); 0 (CFTR protein, human); 0 (Carbonic Anhydrase Inhibitors); 0 (Chlorides); 0 (Chromones); 0 (Isoquinolines); 0 (Morpholines); 0 (Parathyroid Hormone); 0 (Potassium Channels, Calcium-Activated); 0 (Pyrazoles); 0 (Sulfonamides); 0 (TRAM 34); 0 (tenapanor); 0VK51DA1T2 (barium chloride); 126880-72-6 (Cystic Fibrosis Transmembrane Conductance Regulator); 1F7A44V6OU (Colforsin); 27YLU75U4W (Phosphorus); 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase); G07GZ97H65 (Clotrimazole); O3FX965V0I (Acetazolamide); RWP5GA015D (Potassium); SY7Q814VUP (Calcium); XVA4O219QW (wortmannin)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170802
[Lr] Data última revisão:
170802
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170512
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00010.2017


  5 / 2188 MEDLINE  
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[PMID]:28396535
[Au] Autor:Hu XQ; Dasgupta C; Chen M; Xiao D; Huang X; Han L; Yang S; Xu Z; Zhang L
[Ad] Endereço:Institute for Fetology, First Hospital of Soochow University, Suzhou, China (X.-Q.H., Z.X., L.Z.); Lawrence D. Longo MD Center for Perinatal Biology, Department of Basic Sciences, Loma Linda University School of Medicine, CA (X.-Q.H., C.D., D.X., X.H., Z.X., L.Z.); Department of Chemistry and Bioche
[Ti] Título:Pregnancy Reprograms Large-Conductance Ca -Activated K Channel in Uterine Arteries: Roles of Ten-Eleven Translocation Methylcytosine Dioxygenase 1-Mediated Active Demethylation.
[So] Source:Hypertension;69(6):1181-1191, 2017 Jun.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The large-conductance Ca -activated K (BK ) channel is of critical importance in pregnancy-mediated increase in uterine artery vasodilation and blood flow. The present study tested the hypothesis that active DNA demethylation plays a key role in pregnancy-induced reprogramming and upregulation of BK channel ß1 subunit (BKß1) in uterine arteries. Uterine arteries were isolated from nonpregnant and near-term pregnant sheep. Pregnancy significantly increased the expression of ten-eleven translocation methylcytosine dioxygenase 1 (TET1) in uterine arteries. A half-palindromic estrogen response element was identified at the TET1 promoter, and estrogen treatment increased TET1 promoter activity and TET1 expression in uterine arteries. In accordance, pregnancy and steroid hormone treatment resulted in demethylation of BKß1 promoter by increasing 5-hydroxymethylcytosine and decreasing 5-methylcytosine at the CpG in the Sp1 binding site that is of critical importance in the regulation of the promoter activity and BKß1 expression. Inhibition of TET1 with fumarate significantly decreased BKß1 expression in uterine arteries of pregnant animals and blocked steroid hormone-induced upregulation of BKß1. Functionally, fumarate treatment inhibited pregnancy and steroid hormone-induced increases in BK channel current density and BK channel-mediated relaxations. In addition, fumarate blocked pregnancy and steroid hormone-induced decrease in pressure-dependent myogenic tone of the uterine artery. The results demonstrate a novel mechanism of estrogen-mediated active DNA demethylation in reprogramming of BK channel expression and function in the adaption of uterine circulation during pregnancy.
[Mh] Termos MeSH primário: 5-Metilcitosina/metabolismo
Dioxigenases/metabolismo
Metilação/efeitos dos fármacos
Canais de Potássio Cálcio-Ativados/sangue
Prenhez
Artéria Uterina/metabolismo
[Mh] Termos MeSH secundário: Análise de Variância
Animais
Western Blotting
Estradiol/farmacologia
Estrogênios/farmacologia
Feminino
Transporte de Íons
Gravidez
Proteína Quinase C/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Ovinos
Coleta de Tecidos e Órgãos
Regulação para Cima
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogens); 0 (Potassium Channels, Calcium-Activated); 4TI98Z838E (Estradiol); 6R795CQT4H (5-Methylcytosine); EC 1.13.11.- (Dioxygenases); EC 2.7.11.13 (Protein Kinase C)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170816
[Lr] Data última revisão:
170816
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170412
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09059


  6 / 2188 MEDLINE  
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[PMID]:28302447
[Au] Autor:Tanaka S; Ono Y; Sakamoto K
[Ad] Endereço:Department of Pharmacology, Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima, Fukushima, 960-1295, Japan.
[Ti] Título:DCEBIO facilitates myogenic differentiation via intermediate conductance Ca activated K channel activation in C2C12 myoblasts.
[So] Source:J Pharmacol Sci;133(4):276-279, 2017 Apr.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Membrane hyperpolarization is suggested to be a trigger for skeletal muscle differentiation. We investigated whether DCEBIO, an opener of the small/intermediate conductance Ca activated K (SK /IK ) channels, increase myogenic differentiation in C2C12 skeletal myoblasts. DCEBIO significantly increased myotube formation, protein expression level of myosin heavy chain II, and mRNA expression level of myogenin in C2C12 myoblasts cultured in differentiation medium. DCEBIO induced myotube formation and hyperpolarization were reduced by the IK channel blocker TRAM-34, but not by the SK channel blocker apamin. These findings show that DCEBIO increases myogenic differentiation by activating IK channels.
[Mh] Termos MeSH primário: Benzimidazóis/farmacologia
Diferenciação Celular/efeitos dos fármacos
Mioblastos/citologia
Canais de Potássio Cálcio-Ativados/efeitos dos fármacos
[Mh] Termos MeSH secundário: Apamina/farmacologia
Células Cultivadas
Expressão Gênica/efeitos dos fármacos
Seres Humanos
Fibras Musculares Esqueléticas/efeitos dos fármacos
Músculo Esquelético/citologia
Mioblastos/metabolismo
Miogenina/genética
Miogenina/metabolismo
Cadeias Pesadas de Miosina/genética
Cadeias Pesadas de Miosina/metabolismo
Canais de Potássio Cálcio-Ativados/antagonistas & inibidores
Pirazóis/farmacologia
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-one); 0 (Benzimidazoles); 0 (Myogenin); 0 (Potassium Channels, Calcium-Activated); 0 (Pyrazoles); 0 (RNA, Messenger); 0 (TRAM 34); 24345-16-2 (Apamin); EC 3.6.4.1 (Myosin Heavy Chains)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE


  7 / 2188 MEDLINE  
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[PMID]:28267675
[Au] Autor:Kaczmarek LK; Aldrich RW; Chandy KG; Grissmer S; Wei AD; Wulff H
[Ad] Endereço:Departments of Pharmacology and Cellular and Molecular Physiology, Yale School of Medicine, New Haven, Connecticut (L.K.K.); Center for Learning and Memory and Department of Neuroscience, University of Texas at Austin, Austin, Texas (R.W.A.); Laboratory of Molecular Physiology in the Infection and I
[Ti] Título:International Union of Basic and Clinical Pharmacology. C. Nomenclature and Properties of Calcium-Activated and Sodium-Activated Potassium Channels.
[So] Source:Pharmacol Rev;69(1):1-11, 2017 Jan.
[Is] ISSN:1521-0081
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A subset of potassium channels is regulated primarily by changes in the cytoplasmic concentration of ions, including calcium, sodium, chloride, and protons. The eight members of this subfamily were originally all designated as calcium-activated channels. More recent studies have clarified the gating mechanisms for these channels and have documented that not all members are sensitive to calcium. This article describes the molecular relationships between these channels and provides an introduction to their functional properties. It also introduces a new nomenclature that differentiates between calcium- and sodium-activated potassium channels.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Cloretos/metabolismo
Ativação do Canal Iônico
Canais de Potássio Cálcio-Ativados/classificação
Canais de Potássio Cálcio-Ativados/metabolismo
Canais de Potássio/classificação
Canais de Potássio/metabolismo
Sódio/metabolismo
Terminologia como Assunto
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Canais de Potássio Ativados por Cálcio de Condutância Intermediária/classificação
Canais de Potássio Ativados por Cálcio de Condutância Intermediária/metabolismo
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/classificação
Subunidades alfa do Canal de Potássio Ativado por Cálcio de Condutância Alta/metabolismo
Masculino
Espermatozoides/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Chlorides); 0 (Intermediate-Conductance Calcium-Activated Potassium Channels); 0 (KCNMA1 protein, human); 0 (KCNN4 protein, human); 0 (Large-Conductance Calcium-Activated Potassium Channel alpha Subunits); 0 (Potassium Channels); 0 (Potassium Channels, Calcium-Activated); 9NEZ333N27 (Sodium); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170605
[Lr] Data última revisão:
170605
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE
[do] DOI:10.1124/pr.116.012864


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[PMID]:28254750
[Au] Autor:Louie JC; Fujii N; Meade RD; McNeely BD; Kenny GP
[Ad] Endereço:Human and Environmental Physiology Research Unit, School of Human Kinetics, University of Ottawa, Ottawa, Ontario, Canada; and.
[Ti] Título:The roles of K , K , and K channels in regulating cutaneous vasodilation and sweating during exercise in the heat.
[So] Source:Am J Physiol Regul Integr Comp Physiol;312(5):R821-R827, 2017 May 01.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We recently showed the varying roles of Ca -activated (K ), ATP-sensitive (K ), and voltage-gated (K ) K channels in regulating cholinergic cutaneous vasodilation and sweating in normothermic conditions. However, it is unclear whether the respective contributions of these K channels remain intact during dynamic exercise in the heat. Eleven young (23 ± 4 yr) men completed a 30-min exercise bout at a fixed rate of metabolic heat production (400 W) followed by a 40-min recovery period in the heat (35°C, 20% relative humidity). Cutaneous vascular conductance (CVC) and local sweat rate were assessed at four forearm skin sites perfused via intradermal microdialysis with: ) lactated Ringer solution (control); ) 50 mM tetraethylammonium (nonspecific K channel blocker); ) 5 mM glybenclamide (selective K channel blocker); or ) 10 mM 4-aminopyridine (nonspecific K channel blocker). Responses were compared at baseline and at 10-min intervals during and following exercise. K channel inhibition resulted in greater CVC versus control at end exercise ( = 0.04) and 10 and 20 min into recovery (both < 0.01). K channel blockade attenuated CVC compared with control during baseline ( = 0.04), exercise (all ≤ 0.04), and 10 min into recovery ( = 0.02). No differences in CVC were observed with K channel inhibition during baseline ( = 0.15), exercise (all ≥ 0.06), or recovery (all ≥ 0.14). With the exception of K channel inhibition augmenting sweating during baseline ( = 0.04), responses were similar to control with all K channel blockers during each time period (all ≥ 0.07). We demonstrated that K and K channels contribute to the regulation of cutaneous vasodilation during rest and/or exercise and recovery in the heat.
[Mh] Termos MeSH primário: Exercício/fisiologia
Resposta ao Choque Térmico/fisiologia
Canais de Potássio/metabolismo
Fenômenos Fisiológicos da Pele
Sudorese/fisiologia
Vasodilatação/fisiologia
[Mh] Termos MeSH secundário: Velocidade do Fluxo Sanguíneo/fisiologia
Seres Humanos
Canais KATP/metabolismo
Masculino
Canais de Potássio Cálcio-Ativados/metabolismo
Canais de Potássio de Abertura Dependente da Tensão da Membrana/metabolismo
Fluxo Sanguíneo Regional/fisiologia
Pele/irrigação sanguínea
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (KATP Channels); 0 (Potassium Channels); 0 (Potassium Channels, Calcium-Activated); 0 (Potassium Channels, Voltage-Gated)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00507.2016


  9 / 2188 MEDLINE  
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[PMID]:28223151
[Au] Autor:Ruamyod K; Watanapa WB; Shayakul C
[Ad] Endereço:Department of Physiology Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand. Electronic address: katesirin.ruy@mahidol.ac.th.
[Ti] Título:Testosterone rapidly increases Ca -activated K currents causing hyperpolarization in human coronary artery endothelial cells.
[So] Source:J Steroid Biochem Mol Biol;168:118-126, 2017 Apr.
[Is] ISSN:1879-1220
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Testosterone has endothelium-dependent vasodilatory effects on the coronary artery, with some reports suggesting endothelial ion channel involvement. This study employed the whole-cell patch clamp technique to investigate the effect of testosterone on ion channels in human coronary artery endothelial cells (HCAECs) and the mechanisms involved. We found that 0.03-3µM testosterone significantly induced a rapid, concentration-dependent increase in total HCAEC current (EC , 71.96±1.66nM; maximum increase, 59.13±8.37%; mean±SEM). The testosterone-enhanced currents consisted of small- and large-conductance Ca -activated K currents (SK and BK currents), but not Cl and nonselective cation currents. Either a non-permeant testosterone conjugate or the non-aromatizable androgen dihydrotestosterone (DHT) could increase HCAEC currents as well. The androgen receptor antagonist flutamide prevented this testosterone, testosterone conjugate, and DHT effect, while the estrogen receptor antagonist fulvestrant did not. Incubating HCAECs with pertussis toxin or protein kinase A inhibitor H-89 largely inhibited the testosterone effect, while pre-incubation with phospholipase C inhibitor U-73122, prostacyclin inhibitor indomethacin, nitric oxide synthase inhibitor L-NAME or cytochrome P450 inhibitor MS-PPOH, did not. Finally, testosterone application induced HCAEC hyperpolarization within minutes; this effect was prevented by SK and BK current inhibitors apamin and iberiotoxin. This is the first electrophysiological demonstration of androgen-induced K current increase, leading to hyperpolarization, in any endothelial cell, and the first report of SK as a testosterone target. Our data show that testosterone rapidly increased whole-cell HCAEC SK and BK currents via a surface androgen receptor, G protein, and protein kinase A. This mechanism may explain rapid testosterone-induced coronary vasodilation seen in vivo.
[Mh] Termos MeSH primário: Vasos Coronários/citologia
Células Endoteliais/metabolismo
Subunidades alfa Gi-Go de Proteínas de Ligação ao GTP/metabolismo
Canais de Potássio Cálcio-Ativados/metabolismo
Testosterona/sangue
[Mh] Termos MeSH secundário: Androgênios/química
Apamina/química
Linhagem Celular
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Células Endoteliais/efeitos dos fármacos
Epoprostenol/antagonistas & inibidores
Estrenos/química
Seres Humanos
Indometacina/química
NG-Nitroarginina Metil Éster/química
Óxido Nítrico Sintase/química
Pirrolidinonas/química
Receptores Androgênicos/metabolismo
Transdução de Sinais
Testosterona/química
Vasodilatação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androgens); 0 (Estrenes); 0 (Potassium Channels, Calcium-Activated); 0 (Pyrrolidinones); 0 (Receptors, Androgen); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); 24345-16-2 (Apamin); 3XMK78S47O (Testosterone); DCR9Z582X0 (Epoprostenol); EC 1.14.13.39 (Nitric Oxide Synthase); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); EC 3.6.5.1 (GTP-Binding Protein alpha Subunits, Gi-Go); V55S2QJN2X (NG-Nitroarginine Methyl Ester); XXE1CET956 (Indomethacin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170704
[Lr] Data última revisão:
170704
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE


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[PMID]:28130333
[Au] Autor:Parikh J; Kapela A; Tsoukias NM
[Ad] Endereço:Department of Biomedical Engineering, Florida International University, Miami, Florida; and.
[Ti] Título:Can endothelial hemoglobin-α regulate nitric oxide vasodilatory signaling?
[So] Source:Am J Physiol Heart Circ Physiol;312(4):H854-H866, 2017 Apr 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We used mathematical modeling to investigate nitric oxide (NO)-dependent vasodilatory signaling in the arteriolar wall. Detailed continuum cellular models of calcium (Ca ) dynamics and membrane electrophysiology in smooth muscle and endothelial cells (EC) were coupled with models of NO signaling and biotransport in an arteriole. We used this theoretical approach to examine the role of endothelial hemoglobin-α (Hbα) as a modulator of NO-mediated myoendothelial feedback, as previously suggested in Straub et al. ( 491: 473-477, 2012). The model considers enriched expression of inositol 1,4,5-triphosphate receptors (IP Rs), endothelial nitric oxide synthase (eNOS) enzyme, Ca -activated potassium (K ) channels and Hbα in myoendothelial projections (MPs) between the two cell layers. The model suggests that NO-mediated myoendothelial feedback is plausible if a significant percentage of eNOS is localized within or near the myoendothelial projection. Model results show that the ability of Hbα to regulate the myoendothelial feedback is conditional to its colocalization with eNOS near MPs at concentrations in the high nanomolar range (>0.2 µM or 24,000 molecules). Simulations also show that the effect of Hbα observed in in vitro experimental studies may overestimate its contribution in vivo, in the presence of blood perfusion. Thus, additional experimentation is required to quantify the presence and spatial distribution of Hbα in the EC, as well as to test that the strong effect of Hbα on NO signaling seen in vitro, translates also into a physiologically relevant response in vivo. Mathematical modeling shows that although regulation of nitric oxide signaling by hemoglobin-α (Hbα) is plausible, it is conditional to its presence in significant concentrations colocalized with endothelial nitric oxide synthase in myoendothelial projections. Additional experimentation is required to test that the strong effect of Hbα seen in vitro translates into a physiologically relevant response in vivo.
[Mh] Termos MeSH primário: Endotélio Vascular/fisiologia
Hemoglobina A/fisiologia
Óxido Nítrico/fisiologia
Transdução de Sinais/fisiologia
Vasodilatação/fisiologia
[Mh] Termos MeSH secundário: Algoritmos
Simulação por Computador
Eritrócitos/efeitos dos fármacos
Retroalimentação Fisiológica
Seres Humanos
Receptores de Inositol 1,4,5-Trifosfato/efeitos dos fármacos
Modelos Teóricos
Óxido Nítrico Sintase Tipo III/biossíntese
Canais de Potássio Cálcio-Ativados/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inositol 1,4,5-Trisphosphate Receptors); 0 (Potassium Channels, Calcium-Activated); 31C4KY9ESH (Nitric Oxide); 9034-51-9 (Hemoglobin A); EC 1.14.13.39 (NOS3 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type III)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170728
[Lr] Data última revisão:
170728
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170129
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00315.2016



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