Base de dados : MEDLINE
Pesquisa : D02.092.877.250.592.400 [Categoria DeCS]
Referências encontradas : 1759 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 176 ir para página                         

  1 / 1759 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28642099
[Au] Autor:Crossley DA; Crossley JL; Smith C; Harfush M; Sánchez-Sánchez H; Garduño-Paz MV; Méndez-Sánchez JF
[Ad] Endereço:Department of Biological Sciences, University of North Texas, Denton, TX, USA. Electronic address: dane.crossley@unt.edu.
[Ti] Título:Developmental cardiovascular physiology of the olive ridley sea turtle (Lepidochelys olivacea).
[So] Source:Comp Biochem Physiol A Mol Integr Physiol;211:69-76, 2017 Sep.
[Is] ISSN:1531-4332
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Our understanding of reptilian cardiovascular development and regulation has increased substantially for two species the American alligator (Alligator mississippiensis) and the common snapping turtle (Chelydra serpentina) during the past two decades. However, what we know about cardiovascular maturation in many other species remains poorly understood or unknown. Embryonic sea turtles have been studied to understand the maturation of metabolic function, but these studies have not addressed the cardiovascular system. Although prior studies have been pivotal in characterizing development, and factors that influence it, the development of cardiovascular function, which supplies metabolic function, is unknown in sea turtles. During our investigation we focused on quantifying how cardiovascular morphological and functional parameters change, to provide basic knowledge of development in the olive ridley sea turtle (Lepidochelys olivacea). Embryonic mass, as well as mass of the heart, lungs, liver, kidney, and brain increased during turtle embryo development. Although heart rate was constant during this developmental period, arterial pressure approximately doubled. Further, while embryonic olive ridley sea turtles lacked cholinergic tone on heart rate, there was a pronounced beta adrenergic tone on heart rate that decreased in strength at 90% of incubation. This beta adrenergic tone may be partially originating from the sympathetic nervous system at 90% of incubation, with the majority originating from circulating catecholamines. Data indicates that olive ridley sea turtles share traits of embryonic functional cardiovascular maturation with the American alligator (Alligator mississippiensis) but not the common snapping turtle (Chelydra serpentina).
[Mh] Termos MeSH primário: Sistema Cardiovascular/embriologia
Tartarugas/embriologia
[Mh] Termos MeSH secundário: Acetilcolina/administração & dosagem
Animais
Frequência Cardíaca
Hexametônio/administração & dosagem
Cloreto de Sódio/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
3C9PSP36Z2 (Hexamethonium); 451W47IQ8X (Sodium Chloride); N9YNS0M02X (Acetylcholine)
[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:170624
[St] Status:MEDLINE


  2 / 1759 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Vassallo, Dalton Valentim
Texto completo
[PMID]:28499935
[Au] Autor:Toscano CM; Simões MR; Alonso MJ; Salaices M; Vassallo DV; Fioresi M
[Ad] Endereço:Department of Physiological Sciences, Federal University of Espirito Santo, Vitória, ES CEP 29040-091, Brazil. Electronic address: cindymedici@gmail.com.
[Ti] Título:Sub-chronic lead exposure produces ß -adrenoceptor downregulation decreasing arterial pressure reactivity in rats.
[So] Source:Life Sci;180:93-101, 2017 Jul 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Lead is considered a causative factor for hypertension and other cardiovascular diseases. AIMS: To investigate the effects of sub-chronic lead exposure on blood pressure reactivity and cardiac ß -adrenoceptor activity and to evaluate whether the effects found in vitro are similar to those found in vivo. MAIN METHODS: Male Wistar rats were randomly distributed into two groups: control rats (Ct) and rats administered drinking water containing 100ppm lead (Pb) for 30days. KEY FINDINGS: Blood pressure in the Pb rats increased starting from the first week of treatment until the end of the study [systolic blood pressure, Ct: 122±4 vs. Pb: 143±3mmHg; diastolic blood pressure, Ct: 63±4 vs. Pb: 84±4mmHg]. The heart rate was also increased (Ct: 299±11 vs. Pb: 365±11bpm), but the pressure reactivity to phenylephrine was decreased. Losartan and hexamethonium exhibited a greater reduction in blood pressure of Pb rats than in the Ct rats. Isoproterenol increased the left ventricular systolic and end-diastolic pressure, and heart rate only in Ct rats, suggesting that lead induced ß -adrenoceptor downregulation. Indomethacin reduced the blood pressure and heart rate in the Pb rats, suggesting the involvement of cyclooxygenase-derived products (which are associated with reduced nitric oxide bioavailability) in this process. SIGNIFICANCE: These findings offer further evidence that the effects of sub-chronic lead exposure in vitro can be reproduced in vivo-even at low concentrations-thus triggering mechanisms for the development of hypertension. Therefore, lead should be considered an environmental risk factor for cardiovascular disease.
[Mh] Termos MeSH primário: Pressão Arterial/efeitos dos fármacos
Hipertensão/induzido quimicamente
Chumbo/toxicidade
Receptores Adrenérgicos beta 1/genética
[Mh] Termos MeSH secundário: Animais
Doenças Cardiovasculares/induzido quimicamente
Regulação para Baixo
Frequência Cardíaca/efeitos dos fármacos
Hexametônio/farmacologia
Indometacina/farmacologia
Isoproterenol/farmacologia
Chumbo/administração & dosagem
Losartan/farmacologia
Masculino
Óxido Nítrico/metabolismo
Fenilefrina/farmacologia
Ratos
Ratos Wistar
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Adrenergic, beta-1); 1WS297W6MV (Phenylephrine); 2P299V784P (Lead); 31C4KY9ESH (Nitric Oxide); 3C9PSP36Z2 (Hexamethonium); JMS50MPO89 (Losartan); L628TT009W (Isoproterenol); XXE1CET956 (Indomethacin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170514
[St] Status:MEDLINE


  3 / 1759 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27565052
[Au] Autor:Khanmoradi M; Nasimi A
[Ad] Endereço:Department of physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.
[Ti] Título:Angiotensin II in the paraventricular nucleus stimulates sympathetic outflow to the cardiovascular system and make vasopressin release in rat.
[So] Source:Neurosci Lett;632:98-103, 2016 Oct 06.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The hypothalamic paraventricular nucleus (PVN) plays essential roles in neuroendocrine and autonomic functions, including cardiovascular regulation. It was shown that microinjection of angiotensin II (AngII) into the PVN produced a pressor response. In this study, we explored the probable mechanisms of this pressor response. AngII was microinjected into the PVN and cardiovascular responses were recorded. Then, the responses were re-tested after systemic injection of a ganglionic blocker, Hexamethonium, or a vasopressin V1 receptor blocker. Hexamethonium pretreatment (i.v.) greatly and significantly attenuated the pressor response to AngII, with no significant effect on heart rate, indicating that the sympathetic system is involved in the cardiovascular effect of AngII in the PVN. Systemic pretreatment (i.v.) with V1 antagonist greatly and significantly attenuated the pressor response to AngII, with no significant effect on heart rate, indicating that vasopressin release is involved in the cardiovascular effect of AngII in the PVN. Overall, we found that AngII microinjected into the PVN produced a pressor response mediated by the sympathetic system and vasopressin release, indicating that other than circulating AngII, endogenous AngII of the PVN increases the vasopressin release from the PVN.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Sistema Cardiovascular/efeitos dos fármacos
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Sistema Nervoso Simpático/efeitos dos fármacos
Vasopressinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Antagonistas de Receptores de Hormônios Antidiuréticos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Sistema Cardiovascular/metabolismo
Bloqueadores Ganglionares/farmacologia
Frequência Cardíaca/efeitos dos fármacos
Hexametônio/farmacologia
Masculino
Microinjeções
Núcleo Hipotalâmico Paraventricular/metabolismo
Ratos
Ratos Wistar
Sistema Nervoso Simpático/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidiuretic Hormone Receptor Antagonists); 0 (Ganglionic Blockers); 11000-17-2 (Vasopressins); 11128-99-7 (Angiotensin II); 3C9PSP36Z2 (Hexamethonium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170808
[Lr] Data última revisão:
170808
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160828
[St] Status:MEDLINE


  4 / 1759 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27342878
[Au] Autor:Stoyek MR; Quinn TA; Croll RP; Smith FM
[Ad] Endereço:Department of Medical Neuroscience, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada; and.
[Ti] Título:Zebrafish heart as a model to study the integrative autonomic control of pacemaker function.
[So] Source:Am J Physiol Heart Circ Physiol;311(3):H676-88, 2016 Sep 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cardiac pacemaker sets the heart's primary rate, with pacemaker discharge controlled by the autonomic nervous system through intracardiac ganglia. A fundamental issue in understanding the relationship between neural activity and cardiac chronotropy is the identification of neuronal populations that control pacemaker cells. To date, most studies of neurocardiac control have been done in mammalian species, where neurons are embedded in and distributed throughout the heart, so they are largely inaccessible for whole-organ, integrative studies. Here, we establish the isolated, innervated zebrafish heart as a novel alternative model for studies of autonomic control of heart rate. Stimulation of individual cardiac vagosympathetic nerve trunks evoked bradycardia (parasympathetic activation) and tachycardia (sympathetic activation). Simultaneous stimulation of both vagosympathetic nerve trunks evoked a summative effect. Effects of nerve stimulation were mimicked by direct application of cholinergic and adrenergic agents. Optical mapping of electrical activity confirmed the sinoatrial region as the site of origin of normal pacemaker activity and identified a secondary pacemaker in the atrioventricular region. Strong vagosympathetic nerve stimulation resulted in a shift in the origin of initial excitation from the sinoatrial pacemaker to the atrioventricular pacemaker. Putative pacemaker cells in the sinoatrial and atrioventricular regions expressed adrenergic ß2 and cholinergic muscarinic type 2 receptors. Collectively, we have demonstrated that the zebrafish heart contains the accepted hallmarks of vertebrate cardiac control, establishing this preparation as a viable model for studies of integrative physiological control of cardiac function by intracardiac neurons.
[Mh] Termos MeSH primário: Nó Atrioventricular/inervação
Coração/inervação
Sistema Nervoso Parassimpático/fisiologia
Nó Sinoatrial/inervação
Sistema Nervoso Simpático/fisiologia
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos beta/farmacologia
Animais
Nó Atrioventricular/efeitos dos fármacos
Nó Atrioventricular/fisiologia
Nó Atrioventricular/fisiopatologia
Atropina/farmacologia
Sistema Nervoso Autônomo/efeitos dos fármacos
Sistema Nervoso Autônomo/fisiologia
Bradicardia/fisiopatologia
Eletrocardiografia
Coração/efeitos dos fármacos
Coração/fisiologia
Coração/fisiopatologia
Frequência Cardíaca
Hexametônio/farmacologia
Preparação de Coração Isolado
Isoproterenol/farmacologia
Modelos Animais
Muscarina/farmacologia
Agonistas Muscarínicos/farmacologia
Antagonistas Muscarínicos/farmacologia
Nicotina/farmacologia
Agonistas Nicotínicos/farmacologia
Antagonistas Nicotínicos/farmacologia
Sistema Nervoso Parassimpático/efeitos dos fármacos
Receptor Muscarínico M2/metabolismo
Receptores Adrenérgicos beta 2/metabolismo
Nó Sinoatrial/efeitos dos fármacos
Nó Sinoatrial/fisiologia
Nó Sinoatrial/fisiopatologia
Sistema Nervoso Simpático/efeitos dos fármacos
Simpatomiméticos/farmacologia
Taquicardia/fisiopatologia
Timolol/farmacologia
Estimulação do Nervo Vago
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Muscarinic Agonists); 0 (Muscarinic Antagonists); 0 (Nicotinic Agonists); 0 (Nicotinic Antagonists); 0 (Receptor, Muscarinic M2); 0 (Receptors, Adrenergic, beta-2); 0 (Sympathomimetics); 3C9PSP36Z2 (Hexamethonium); 6M3C89ZY6R (Nicotine); 7C0697DR9I (Atropine); 7T101UWZ5W (Muscarine); 817W3C6175 (Timolol); L628TT009W (Isoproterenol)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170902
[Lr] Data última revisão:
170902
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160626
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00330.2016


  5 / 1759 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27098245
[Au] Autor:Kanashiro A; Talbot J; Peres RS; Pinto LG; Bassi GS; Cunha TM; Cunha FQ
[Ad] Endereço:Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, SP, Brazil. alex_bioquimica@yahoo.com.br.
[Ti] Título:Neutrophil Recruitment and Articular Hyperalgesia in Antigen-Induced Arthritis are Modulated by the Cholinergic Anti-Inflammatory Pathway.
[So] Source:Basic Clin Pharmacol Toxicol;119(5):453-457, 2016 Nov.
[Is] ISSN:1742-7843
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The cholinergic anti-inflammatory pathway (CAP) is a complex neuroimmune mechanism triggered by the central nervous system to regulate peripheral inflammatory responses. Understanding the role of CAP in the pathogenesis of rheumatoid arthritis (RA) could help develop new therapeutic strategies for this disease. Therefore, we investigated the participation of this neuroimmune pathway on the progression of experimental arthritis. Using antigen-induced arthritis (AIA) model, we investigated in mice the effects of vagotomy or the pharmacological treatments with hexamethonium (peripheral nicotinic receptor antagonist), methylatropine (peripheral muscarinic receptor antagonist) or neostigmine (peripheral acetylcholinesterase inhibitor) on AIA progression. Unilateral cervical vagotomy was performed 1 week before the immunization protocol with methylated bovine serum albumin (mBSA), while drug administration was conducted during the period of immunization. On day 21, 6 hr after the challenge with mBSA injection in the femur-tibial joint, the local neutrophil migration and articular mechanical hyperalgesia were assessed. Herein, we observed that vagotomy or blockade of peripheral nicotinic (but not muscarinic) receptors exacerbated the clinical parameters of this disease. Moreover, peripheral acetylcholinesterase inhibition by neostigmine treatment promoted a reduction of neutrophil recruitment in the knee joint and articular hyperalgesia. Our results demonstrated that peripheral activation of CAP modulates experimental arthritis, providing a pre-clinical evidence of a potential therapeutic strategy for RA.
[Mh] Termos MeSH primário: Artrite Experimental/imunologia
Artrite Reumatoide/imunologia
Neurônios Colinérgicos/imunologia
Vias Eferentes/imunologia
Hiperalgesia/tratamento farmacológico
Neuroimunomodulação/efeitos dos fármacos
Infiltração de Neutrófilos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antígenos/efeitos adversos
Artrite Experimental/tratamento farmacológico
Artrite Experimental/etiologia
Artrite Reumatoide/tratamento farmacológico
Derivados da Atropina/farmacologia
Inibidores da Colinesterase/farmacologia
Hexametônio/farmacologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Antagonistas Muscarínicos/farmacologia
Neostigmina/farmacologia
Antagonistas Nicotínicos/farmacologia
Soroalbumina Bovina
Vagotomia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens); 0 (Atropine Derivatives); 0 (Cholinesterase Inhibitors); 0 (Muscarinic Antagonists); 0 (Nicotinic Antagonists); 0 (methylated bovine serum albumin); 27432CM55Q (Serum Albumin, Bovine); 3982TWQ96G (Neostigmine); 3C9PSP36Z2 (Hexamethonium); 80719I460H (methylatropine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160422
[St] Status:MEDLINE
[do] DOI:10.1111/bcpt.12611


  6 / 1759 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26825997
[Au] Autor:Tangsucharit P; Takatori S; Zamami Y; Goda M; Pakdeechote P; Kawasaki H; Takayama F
[Ad] Endereço:Department of Clinical Pharmaceutical Sciences, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan; Department of Pharmacology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
[Ti] Título:Muscarinic acetylcholine receptor M1 and M3 subtypes mediate acetylcholine-induced endothelium-independent vasodilatation in rat mesenteric arteries.
[So] Source:J Pharmacol Sci;130(1):24-32, 2016 Jan.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The present study investigated pharmacological characterizations of muscarinic acetylcholine receptor (AChR) subtypes involving ACh-induced endothelium-independent vasodilatation in rat mesenteric arteries. Changes in perfusion pressure to periarterial nerve stimulation and ACh were measured before and after the perfusion of Krebs solution containing muscarinic receptor antagonists. Distributions of muscarinic AChR subtypes in mesenteric arteries with an intact endothelium were studied using Western blotting. The expression level of M1 and M3 was significantly greater than that of M2. Endothelium removal significantly decreased expression levels of M2 and M3, but not M1. In perfused mesenteric vascular beds with intact endothelium and active tone, exogenous ACh (1, 10, and 100 nmol) produced concentration-dependent and long-lasting vasodilatations. In endothelium-denuded preparations, relaxation to ACh (1 nmol) disappeared, but ACh at 10 and 100 nmol caused long-lasting vasodilatations, which were markedly blocked by the treatment of pirenzepine (M1 antagonist) or 4-DAMP (M1 and M3 antagonist) plus hexamethonium (nicotinic AChR antagonist), but not methoctramine (M2 and M4 antagonist). These results suggest that muscarinic AChR subtypes, mainly M1, distribute throughout the rat mesenteric arteries, and that activation of M1 and/or M3 which may be located on CGRPergic nerves releases CGRP, causing an endothelium-independent vasodilatation.
[Mh] Termos MeSH primário: Acetilcolina/farmacologia
Endotélio Vascular
Artérias Mesentéricas/efeitos dos fármacos
Receptor Muscarínico M1/fisiologia
Receptor Muscarínico M3/fisiologia
Vasodilatação/efeitos dos fármacos
[Mh] Termos MeSH secundário: Acetilcolina/antagonistas & inibidores
Animais
Peptídeo Relacionado com Gene de Calcitonina/secreção
Relação Dose-Resposta a Droga
Hexametônio/farmacologia
Técnicas In Vitro
Masculino
Artérias Mesentéricas/metabolismo
Piperidinas/farmacologia
Pirenzepina/farmacologia
Ratos Wistar
Receptor Muscarínico M1/antagonistas & inibidores
Receptor Muscarínico M1/metabolismo
Receptor Muscarínico M3/antagonistas & inibidores
Receptor Muscarínico M3/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Piperidines); 0 (Receptor, Muscarinic M1); 0 (Receptor, Muscarinic M3); 3C9PSP36Z2 (Hexamethonium); 3G0285N20N (Pirenzepine); 81405-11-0 (4-diphenylacetoxy-1,1-dimethylpiperidinium); 83652-28-2 (Calcitonin Gene-Related Peptide); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160210
[Lr] Data última revisão:
160210
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160131
[St] Status:MEDLINE


  7 / 1759 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26462538
[Au] Autor:Salaga M; Blomster LV; Piechota-Polanczyk A; Zielinska M; Jacenik D; Cygankiewicz AI; Krajewska WM; Mikkelsen JD; Fichna J
[Ad] Endereço:Department of Biochemistry, Faculty of Medicine, Medical University of Lodz, Lodz, Poland (M.S., A.P.-P., M.Z., J.F.); Neurobiology Research Unit, University Hospital Rigshospitalet, Copenhagen, Denmark (L.V.B., J.D.M.); Department of Cytobiochemistry, Faculty of Biology and Environmental Protection
[Ti] Título:Encenicline, an α7 Nicotinic Acetylcholine Receptor Partial Agonist, Reduces Immune Cell Infiltration in the Colon and Improves Experimental Colitis in Mice.
[So] Source:J Pharmacol Exp Ther;356(1):157-69, 2016 Jan.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The α7 pentamer nicotinic acetylcholine receptors (nAChRs) are a target in transduction of anti-inflammatory signals from the central nervous system to the gastrointestinal (GI) tract. The aim of this study was to investigate the anti-inflammatory action of the novel α7 nAChR partial agonist encenicline and to determine the mechanism underlying its activity. Anti-inflammatory activity of encenicline was evaluated using trinitrobenzenesulfonic acid (TNBS)- and dextran sulfate sodium (DSS)-induced models of colitis. Macroscopic score, ulcer score, colon length and thickness, as well as myeloperoxidase (MPO) activity were recorded. Immunohistochemistry (IHC) was used to measure the infiltration of immune cells in the colon. Furthermore, we employed flow cytometry to determine the effect of encenicline on frequencies of FoxP3(+) and interleukin (IL)-17A(+) T cells in the mouse colon. Encenicline attenuated TNBS- and DSS-induced colitis in mice via α7 nAChRs, as indicated by significantly reduced macroscopic parameters and MPO activity. Treatment with encenicline significantly reduced the infiltration of macrophages, neutrophils, and B cells in the colon of TNBS-treated animals, as indicated by IHC. In the TNBS model encenicline reduced the frequency of FoxP3(+) IL-17A(+) T cells in the colon. In the DSS-model treatment encenicline increased the frequency of FoxP3(+) T cells and reduced IL-17A(+) T cells. Stimulation of α7 nAChR with partial agonist encenicline alleviates colitis via alteration of the number and/or activation status of the immune cells in the gut, emphasizing a potential role of α7 nAChRs as a target for anticolitic drugs.
[Mh] Termos MeSH primário: Colite Ulcerativa/tratamento farmacológico
Colite Ulcerativa/patologia
Colo/patologia
Agonistas Nicotínicos/uso terapêutico
Quinuclidinas/uso terapêutico
Tiofenos/uso terapêutico
Receptor Nicotínico de Acetilcolina alfa7/agonistas
[Mh] Termos MeSH secundário: Animais
Colite Ulcerativa/induzido quimicamente
Sulfato de Dextrana
Citometria de Fluxo
Fatores de Transcrição Forkhead/metabolismo
Hexametônio/farmacologia
Interleucina-17/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Antagonistas Nicotínicos/farmacologia
Peroxidase/metabolismo
Linfócitos T/efeitos dos fármacos
Linfócitos T/metabolismo
Ácido Trinitrobenzenossulfônico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Interleukin-17); 0 (N-(7-chloro-N-quinuclidin-3-yl)benzo(b)thiophene-2-carboxamide); 0 (Nicotinic Agonists); 0 (Nicotinic Antagonists); 0 (Quinuclidines); 0 (Thiophenes); 0 (alpha7 Nicotinic Acetylcholine Receptor); 3C9PSP36Z2 (Hexamethonium); 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid); 9042-14-2 (Dextran Sulfate); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:151209
[Lr] Data última revisão:
151209
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151015
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.115.228205


  8 / 1759 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26397056
[Au] Autor:Li P; Gong JX; Sun W; Zhou B; Kong XQ
[Ad] Endereço:Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
[Ti] Título:Hexamethonium attenuates sympathetic activity and blood pressure in spontaneously hypertensive rats.
[So] Source:Mol Med Rep;12(5):7116-22, 2015 Nov.
[Is] ISSN:1791-3004
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:Sympathetic activity is enhanced in heart failure and hypertensive rats. The aims of the current study were: i) To investigate the association between renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) in response to intravenous injection of the ganglionic blocker hexamethonium; and ii) to determine whether normal Wistar rats and spontaneously hypertensive rats (SHRs) differ in their response to hexamethonium. RSNA and MAP were recorded in anaesthetized rats. Intravenous injection of four doses of hexamethonium significantly reduced the RSNA, MAP and heart rate (HR) in the Wistar rats and SHRs. There were no significant differences in the RSNA, MAP or HR between Wistar rats and SHRs at the two lowest doses of hexamethonium. However, the two highest doses of hexamethonium resulted in a greater reduction in the RSNA and MAP in SHRs compared with Wistar rats. There was a significant positive correlation between the alterations in RSNA and MAP in response to the intravenous injection of hexamethonium in the Wistar rats and SHRs. There were no significant differences in the timing of the maximal effects on RSNA, MAP or HR or in recovery following hexamethonium treatment. These results suggest that there is an association between the RSNA and MAP response to intravenous injection of hexamethonium and that the alterations in MAP in response to hexamethonium may be used to evaluate basal sympathetic nerve activity.
[Mh] Termos MeSH primário: Anti-Hipertensivos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Hexametônio/farmacologia
[Mh] Termos MeSH secundário: Animais
Frequência Cardíaca/efeitos dos fármacos
Masculino
Ratos
Ratos Endogâmicos SHR
Ratos Wistar
Sistema Nervoso Simpático/efeitos dos fármacos
Sistema Nervoso Simpático/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antihypertensive Agents); 3C9PSP36Z2 (Hexamethonium)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151027
[Lr] Data última revisão:
151027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150924
[St] Status:MEDLINE
[do] DOI:10.3892/mmr.2015.4315


  9 / 1759 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26079327
[Au] Autor:Yeganeh F; Ranjbar A; Hatam M; Nasimi A
[Ad] Endereço:Department of Physiology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran.
[Ti] Título:Mechanism of the cardiovascular effects of the GABAA receptors of the ventral tegmental area of the rat brain.
[So] Source:Neurosci Lett;600:193-8, 2015 Jul 23.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The ventral tegmental area (VTA) contains GABA terminals involved in the regulation of the cardiovascular system. Previously, we demonstrated that blocking GABAA but not GABAB receptors produced a pressor response accompanied by marked bradycardia. This study was performed to find the possible mechanisms involved in these responses by blocking ganglionic nicotinic receptors, peripheral muscarinic receptors or peripheral V1 vasopressin receptors. Experiments were performed on urethane anesthetized male Wistar rats. Drugs were microinjected unilaterally into the VTA (100 nl). The average changes in mean arterial pressure (MAP) and heart rate (HR) were compared between pre- and post-treatment using paired t-test. Injection of bicuculline methiodide (BMI), a GABAA antagonist, into the VTA caused a significant increase in MAP and a decrease in HR. Administration (i.v.) of the nicotinic receptor blocker, hexamethonium, enhanced the pressor response but abolished the bradycardic response to BMI, which ruled out involvement of the sympathetic nervous system. Blockade of the peripheral muscarinic receptors by homatropine (i.v.) abolished the bradycardic effect of BMI, but had no effect on the pressor response, indicating that bradycardia was produced by the parasympathetic outflow to the heart. Both the pressor and bradycardic responses to BMI were blocked by V1 receptor antagonist (i.v.), indicating that administration of BMI in the VTA disinhibited the release of vasopressin into the circulation. In conclusion, we demonstrated that GABAergic mechanism of the VTA exerts a tonic inhibition on vasopressin release through activation of GABAA receptors. The sympathetic system is not involved in the decrease of blood pressure by GABA of the VTA.
[Mh] Termos MeSH primário: Pressão Sanguínea/fisiologia
Frequência Cardíaca/fisiologia
Receptores de GABA-A/metabolismo
Área Tegmentar Ventral/metabolismo
[Mh] Termos MeSH secundário: Animais
Antagonistas de Receptores de Hormônios Antidiuréticos/farmacologia
Bicuculina/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Antagonistas de Receptores de GABA-A/farmacologia
Gânglios Autônomos/metabolismo
Frequência Cardíaca/efeitos dos fármacos
Hexametônio/farmacologia
Masculino
Microinjeções
Antagonistas Muscarínicos/farmacologia
Antagonistas Nicotínicos/farmacologia
Ratos Wistar
Tropanos/farmacologia
Vasopressinas/metabolismo
Área Tegmentar Ventral/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antidiuretic Hormone Receptor Antagonists); 0 (GABA-A Receptor Antagonists); 0 (Muscarinic Antagonists); 0 (Nicotinic Antagonists); 0 (Receptors, GABA-A); 0 (Tropanes); 11000-17-2 (Vasopressins); 3C9PSP36Z2 (Hexamethonium); 8QS6WCL55Z (homatropine); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:150718
[Lr] Data última revisão:
150718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150617
[St] Status:MEDLINE


  10 / 1759 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26048072
[Au] Autor:Manuela R; Mario M; Vincenzo R; Filippo R
[Ad] Endereço:Innovative Research Laboratory for Wound Healing, Health Sciences Department, Università del Piemonte Orientale "A. Avogadro", via Solaroli, 17, 28100 Novara, Italy. Electronic address: manuela.rizzi@med.unipmn.it.
[Ti] Título:Nicotine stimulation increases proliferation and matrix metalloproteinases-2 and -28 expression in human dental pulp cells.
[So] Source:Life Sci;135:49-54, 2015 Aug 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Dental pulp is the specialized tissue responsible for maintaining tooth viability. When tooth mineralized matrix is damaged, pulp is exposed to a plethora of environmental stimuli. In particular, in smokers, pulp become exposed to very high concentrations of nicotine. The aim of this study was to investigate the effect of direct nicotine stimulation on human dental pulp cell proliferation. Moreover, as it is known that nicotine could upregulate the expression of matrix metalloproteinases (MMPs), enzymes involved in pulpal inflammation, the effects of nicotine stimulation on MMP-2 and MMP-28 gene expression have also been investigated. MAIN METHODS: Human dental pulp cells were extracted from impacted third molars obtained from healthy patients undergoing routine orthodontic treatments. Such cells were treated with growing concentrations of nicotine in the presence or absence of a nicotine antagonist (hexamethonium chloride) or of a MEK signaling inhibitor (PD98059). Cell proliferation was evaluated by cell counting, while nicotine effects on MMP expression were evaluated by PCR. KEY FINDINGS: The data obtained indicate that nicotine is able to increase human dental pulp cell proliferation by acting through nicotinic cholinergic receptors and downstream MAPK signaling pathway. Moreover, it is also able to increase both MMP-2 and MMP-28 gene expression. SIGNIFICANCE: In summary these results highlight that direct exposure of human dental pulp cells to nicotine results in an inflammatory response, that could have a role in pulpal inflammation onset, a pathological condition that, when ignored, could eventually spread to the surrounding alveolar bone and progress to pulp necrosis.
[Mh] Termos MeSH primário: Polpa Dentária/enzimologia
Estimulantes Ganglionares/farmacologia
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Metaloproteinase 2 da Matriz/biossíntese
Metaloproteinases da Matriz Secretadas/biossíntese
Nicotina/farmacologia
Regulação para Cima/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adolescente
Adulto
Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Polpa Dentária/citologia
Feminino
Flavonoides/farmacologia
Bloqueadores Ganglionares/farmacologia
Hexametônio/farmacologia
Seres Humanos
MAP Quinase Quinase Quinases/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Masculino
Nicotina/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one); 0 (Flavonoids); 0 (Ganglionic Blockers); 0 (Ganglionic Stimulants); 3C9PSP36Z2 (Hexamethonium); 6M3C89ZY6R (Nicotine); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 3.4.24.- (MMP28 protein, human); EC 3.4.24.- (Matrix Metalloproteinases, Secreted); EC 3.4.24.24 (MMP2 protein, human); EC 3.4.24.24 (Matrix Metalloproteinase 2)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150607
[St] Status:MEDLINE



página 1 de 176 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde