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[PMID]:28330378
[Au] Autor:Shen M; Yu M; Li J; Ma L
[Ad] Endereço:a Department of Rehabilitation Medicine , Affiliated Zhongshan Hospital of Dalian University , Dalian , China.
[Ti] Título:Effects of exercise training on kinin receptors expression in rats with myocardial infarction.
[So] Source:Arch Physiol Biochem;123(4):206-211, 2017 Oct.
[Is] ISSN:1744-4160
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The objective of this study is to determine the role of kinin B1 and B2 receptors in exercise-induced cardiac muscle angiogenesis. METHOD: Thirty Wistar rats were randomly assigned to the control group, the myocardial infarction group and the exercise training group (myocardial infarction model was made and received 30 min exercise training on a treadmill). After 4 weeks of experiment, cardiac muscle was harvested. RESULTS: B1 and B2 receptor mRNA and protein levels in the exercise-training group were significantly higher than those in the myocardial infarction group, which were higher than those in the control group. Capillary number in the cardiac muscle also showed the same tendency. There was a correlation between capillary number and B1 receptor protein (not B2 receptor protein) in the all groups. CONCLUSION: Kinin B1 and B2 receptors play roles in exercise-induced cardiac muscle angiogenesis. However, the B1 receptor appears to have a more prominent role.
[Mh] Termos MeSH primário: Cininas/metabolismo
Infarto do Miocárdio/metabolismo
Condicionamento Físico Animal
Receptor B1 da Bradicinina/metabolismo
Receptor B2 da Bradicinina/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Técnicas Imunoenzimáticas
Masculino
Infarto do Miocárdio/genética
Infarto do Miocárdio/patologia
Infarto do Miocárdio/terapia
RNA Mensageiro/genética
Ratos
Ratos Wistar
Reação em Cadeia da Polimerase em Tempo Real
Receptor B1 da Bradicinina/genética
Receptor B2 da Bradicinina/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Kinins); 0 (RNA, Messenger); 0 (Receptor, Bradykinin B1); 0 (Receptor, Bradykinin B2)
[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:170324
[St] Status:MEDLINE
[do] DOI:10.1080/13813455.2017.1302962


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[PMID]:27988430
[Au] Autor:Dutra RC
[Ad] Endereço:Laboratory of Autoimmunity and Immunopharmacology, Department of Health Sciences, Center Araranguá, Universidade Federal de Santa Catarina, Araranguá, SC, Brazil. Electronic address: rafaelcdutra@gmail.com.
[Ti] Título:Kinin receptors: Key regulators of autoimmunity.
[So] Source:Autoimmun Rev;16(2):192-207, 2017 Feb.
[Is] ISSN:1873-0183
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The central function of the immune system is to protect the host from environmental agents such as microbes or chemicals, thereby preserving the integrity of the body, and preventing the onset of illness and infection. Moreover, the immune system is constantly challenged to discriminate self vs. non-self and mediate the correct response, a phenomenon called self-tolerance. The failure of mechanisms responsible for self-tolerance and induction of an immune response against components of the self, induces autoimmunity and culminates however, in several autoimmune diseases. The precise etiology of autoimmune diseases is not known, although the classic sign of an autoimmune disease is inflammation. In this context, kinins are a family of peptides involved in different physiological and pathological states, comprising inflammatory, vascular and pain processes, and are highly relevant as well as to a variety of diseases including hypertension, kidney diseases, Alzheimer's disease, cancer, obesity, epilepsy and traumatic injuries. These kinin effects are mediated by two related G-protein-coupled receptors named the bradykinin receptors (BKRs), B1 and B2. The kallikrein-kinin system (KKS) and their receptors appear to be involved in both the development and progression of autoimmune diseases, suggesting that modulators of BKRs, administered in monotherapy or in combination with existing therapies, may represent a potential new venue for an effective autoimmune disease treatment. This review article highlights historical and recent progress in understanding the role of BKRs as potential therapeutics for a number of autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, type I diabetes mellitus, inflammatory bowel diseases, and others.
[Mh] Termos MeSH primário: Autoimunidade/imunologia
Inflamação/fisiopatologia
Sistema Calicreína-Cinina/imunologia
Cininas/imunologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Kinins)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161219
[St] Status:MEDLINE


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[PMID]:27914700
[Au] Autor:Kahn R; Mossberg M; Ståhl AL; Johansson K; Lopatko Lindman I; Heijl C; Segelmark M; Mörgelin M; Leeb-Lundberg LM; Karpman D
[Ad] Endereço:Department of Pediatrics, Clinical Sciences Lund, Lund University, Lund, Sweden.
[Ti] Título:Microvesicle transfer of kinin B1-receptors is a novel inflammatory mechanism in vasculitis.
[So] Source:Kidney Int;91(1):96-105, 2017 Jan.
[Is] ISSN:1523-1755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:During vasculitis, activation of the kinin system induces inflammation, whereby the kinin B1-receptor is expressed and activated after ligand binding. Additionally, activated blood cells release microvesicles into the circulation. Here we determined whether leukocyte-derived microvesicles bear B1-kinin receptors during vasculitis, and if microvesicles transfer functional B1-receptors to recipient cells, thus promoting inflammation. By flow cytometry, plasma from patients with vasculitis were found to contain high levels of leukocyte-derived microvesicles bearing B1-receptors. Importantly, renal biopsies from two patients with vasculitis showed leukocyte-derived microvesicles bearing B1-receptors docking on glomerular endothelial cells providing in vivo relevance. Microvesicles derived from B1-receptor-transfected human embryonic kidney cells transferred B1-receptors to wild-type human embryonic kidney cells, lacking the receptor, and to glomerular endothelial cells. The transferred B1-receptors induced calcium influx after B1-receptor agonist stimulation: a response abrogated by a specific B1-receptor antagonist. Microvesicles derived from neutrophils also transferred B1-receptors to wild-type human embryonic kidney cells and induced calcium influx after stimulation. Thus, we found a novel mechanism by which microvesicles transfer functional receptors and promote kinin-associated inflammation.
[Mh] Termos MeSH primário: Bradicinina/metabolismo
Micropartículas Derivadas de Células/metabolismo
Inflamação/metabolismo
Rim/metabolismo
Receptor B1 da Bradicinina/metabolismo
Vasculite/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Cálcio
Linhagem Celular
Criança
Células Endoteliais/metabolismo
Feminino
Citometria de Fluxo
Seres Humanos
Rim/citologia
Cininas
Leucócitos/metabolismo
Masculino
Meia-Idade
Neutrófilos/metabolismo
Receptor B1 da Bradicinina/sangue
Receptor B1 da Bradicinina/genética
Transfecção
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Kinins); 0 (Receptor, Bradykinin B1); S8TIM42R2W (Bradykinin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161205
[St] Status:MEDLINE


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[PMID]:27782319
[Au] Autor:Ekdahl KN; Teramura Y; Hamad OA; Asif S; Duehrkop C; Fromell K; Gustafson E; Hong J; Kozarcanin H; Magnusson PU; Huber-Lang M; Garred P; Nilsson B
[Ad] Endereço:Department of Immunology, Genetics and Pathology (IGP), Rudbeck Laboratory C5:3, Uppsala University, Uppsala, Sweden.
[Ti] Título:Dangerous liaisons: complement, coagulation, and kallikrein/kinin cross-talk act as a linchpin in the events leading to thromboinflammation.
[So] Source:Immunol Rev;274(1):245-269, 2016 11.
[Is] ISSN:1600-065X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Innate immunity is fundamental to our defense against microorganisms. Physiologically, the intravascular innate immune system acts as a purging system that identifies and removes foreign substances leading to thromboinflammatory responses, tissue remodeling, and repair. It is also a key contributor to the adverse effects observed in many diseases and therapies involving biomaterials and therapeutic cells/organs. The intravascular innate immune system consists of the cascade systems of the blood (the complement, contact, coagulation, and fibrinolytic systems), the blood cells (polymorphonuclear cells, monocytes, platelets), and the endothelial cell lining of the vessels. Activation of the intravascular innate immune system in vivo leads to thromboinflammation that can be activated by several of the system's pathways and that initiates repair after tissue damage and leads to adverse reactions in several disorders and treatment modalities. In this review, we summarize the current knowledge in the field and discuss the obstacles that exist in order to study the cross-talk between the components of the intravascular innate immune system. These include the use of purified in vitro systems, animal models and various types of anticoagulants. In order to avoid some of these obstacles we have developed specialized human whole blood models that allow investigation of the cross-talk between the various cascade systems and the blood cells. We in particular stress that platelets are involved in these interactions and that the lectin pathway of the complement system is an emerging part of innate immunity that interacts with the contact/coagulation system. Understanding the resulting thromboinflammation will allow development of new therapeutic modalities.
[Mh] Termos MeSH primário: Plaquetas/imunologia
Proteínas do Sistema Complemento/metabolismo
Células Endoteliais/fisiologia
Inflamação/imunologia
Trombose/imunologia
[Mh] Termos MeSH secundário: Animais
Coagulação Sanguínea
Homeostase
Seres Humanos
Imunidade Inata
Calicreínas/metabolismo
Cininas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Kinins); 9007-36-7 (Complement System Proteins); EC 3.4.21.- (Kallikreins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161027
[St] Status:MEDLINE
[do] DOI:10.1111/imr.12471


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[PMID]:27749899
[Au] Autor:Nadur-Andrade N; Dale CS; Oliveira VR; Toniolo EF; Feliciano RD; da Silva JA; Zamuner SR
[Ad] Endereço:Universidade Nove de Julho, São Paulo, São Paulo, Brazil.
[Ti] Título:Analgesic Effect of Photobiomodulation on Bothrops Moojeni Venom-Induced Hyperalgesia: A Mechanism Dependent on Neuronal Inhibition, Cytokines and Kinin Receptors Modulation.
[So] Source:PLoS Negl Trop Dis;10(10):e0004998, 2016 Oct.
[Is] ISSN:1935-2735
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Envenoming induced by Bothrops snakebites is characterized by drastic local tissue damage that involves an intense inflammatory reaction and local hyperalgesia which are not neutralized by conventional antivenom treatment. Herein, the effectiveness of photobiomodulation to reduce inflammatory hyperalgesia induced by Bothrops moojeni venom (Bmv), as well as the mechanisms involved was investigated. METHODOLOGY/PRINCIPAL FINDINGS: Bmv (1 µg) was injected through the intraplantar route in the right hind paw of mice. Mechanical hyperalgesia and allodynia were evaluated by von Frey filaments at different time points after venom injection. Low level laser therapy (LLLT) was applied at the site of Bmv injection at wavelength of red 685 nm with energy density of 2.2 J/cm2 at 30 min and 3 h after venom inoculation. Neuronal activation in the dorsal horn spinal cord was determined by immunohistochemistry of Fos protein and the mRNA expression of IL-6, TNF-α, IL-10, B1 and B2 kinin receptors were evaluated by Real time-PCR 6 h after venom injection. Photobiomodulation reversed Bmv-induced mechanical hyperalgesia and allodynia and decreased Fos expression, induced by Bmv as well as the mRNA levels of IL-6, TNF-α and B1 and B2 kinin receptors. Finally, an increase on IL-10, was observed following LLLT. CONCLUSION/SIGNIFICANCE: These data demonstrate that LLLT interferes with mechanisms involved in nociception and hyperalgesia and modulates Bmv-induced nociceptive signal. The use of photobiomodulation in reducing local pain induced by Bothropic venoms should be considered as a novel therapeutic tool for the treatment of local symptoms induced after bothropic snakebites.
[Mh] Termos MeSH primário: Analgésicos/efeitos adversos
Citocinas/metabolismo
Hiperalgesia/terapia
Cininas/metabolismo
Terapia com Luz de Baixa Intensidade
Neurônios/efeitos dos fármacos
Mordeduras de Serpentes/terapia
Venenos de Serpentes/efeitos adversos
[Mh] Termos MeSH secundário: Analgésicos/administração & dosagem
Animais
Bothrops
Citocinas/genética
Feminino
Seres Humanos
Hiperalgesia/etiologia
Hiperalgesia/genética
Hiperalgesia/metabolismo
Interleucina-10/genética
Interleucina-10/metabolismo
Interleucina-6/genética
Interleucina-6/metabolismo
Cininas/genética
Masculino
Camundongos
Mordeduras de Serpentes/etiologia
Mordeduras de Serpentes/genética
Mordeduras de Serpentes/metabolismo
Venenos de Serpentes/administração & dosagem
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Analgesics); 0 (Cytokines); 0 (Interleukin-6); 0 (Kinins); 0 (Snake Venoms); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10)
[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:161018
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pntd.0004998


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[PMID]:27721576
[Au] Autor:Niewiarowska-Sendo A; Kozik A; Guevara-Lora I
[Ad] Endereço:Department of Analytical Biochemistry, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University in Krakow, Krakow, Poland.
[Ti] Título:Kinin Peptides Enhance Inflammatory and Oxidative Responses Promoting Apoptosis in a Parkinson's Disease Cellular Model.
[So] Source:Mediators Inflamm;2016:4567343, 2016.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kinin peptides ubiquitously occur in nervous tissue and participate in inflammatory processes associated with distinct neurological disorders. These substances have also been demonstrated to promote the oxidative stress. On the other hand, the importance of oxidative stress and inflammation has been emphasized in disorders that involve the neurodegenerative processes such as Parkinson's disease (PD). A growing number of reports have demonstrated the increased expression of kinin receptors in neurodegenerative diseases. In this study, the effect of bradykinin and des-Arg -kallidin, two representative kinin peptides, was analyzed with respect to inflammatory response and induction of oxidative stress in a PD cellular model, obtained after stimulation of differentiated SK-N-SH cells with a neurotoxin, 1-methyl-4-phenylpyridinium. Kinin peptides caused an increased cytokine release and enhanced production of reactive oxygen species and NO by cells. These changes were accompanied by a loss of cell viability and a greater activation of caspases involved in apoptosis progression. Moreover, the neurotoxin and kinin peptides altered the dopamine receptor 2 expression. Kinin receptor expression was also changed by the neurotoxin. These results suggest a mediatory role of kinin peptides in the development of neurodegeneration and may offer new possibilities for its regulation by using specific antagonists of kinin receptors.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Cininas/farmacologia
Doença de Parkinson/metabolismo
[Mh] Termos MeSH secundário: 1-Metil-4-fenilpiridínio/metabolismo
Apoptose/genética
Bradicinina/farmacologia
Diferenciação Celular/efeitos dos fármacos
Diferenciação Celular/genética
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/genética
Citocinas/farmacologia
Seres Humanos
Calidina/análogos & derivados
Calidina/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Kinins); 0 (Reactive Oxygen Species); 342-10-9 (Kallidin); 71800-36-7 (kallidin, des-Arg(10)-); R865A5OY8J (1-Methyl-4-phenylpyridinium); S8TIM42R2W (Bradykinin)
[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:161011
[St] Status:MEDLINE


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[PMID]:27720762
[Au] Autor:Dias L; Rodrigues MA; Inoue BR; Rodrigues RL; Rennó AL; de Souza VB; Torres-Huaco FD; Sousa NC; Stroka A; Melgarejo AR; Hyslop S
[Ad] Endereço:Departamento de Farmacologia, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (UNICAMP), Rua Tessália Vieira de Camargo, 126, Cidade Universitária Zeferino Vaz, 13083-887, Campinas, SP, Brazil.
[Ti] Título:Pharmacological analysis of hemodynamic responses to Lachesis muta (South American bushmaster) snake venom in anesthetized rats.
[So] Source:Toxicon;123:25-44, 2016 Dec 01.
[Is] ISSN:1879-3150
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In this work, we examined some mechanisms involved in the hypotension caused by Lachesis muta (South American bushmaster) venom in anesthetized rats. Venom (1.5 mg/kg, i.v.) caused immediate hypotension that was maximal after 5 min and gradually returned to baseline over 60 min. Pretreatment of rats with the non-selective nitric oxide synthase (NOS) inhibitor N -nitro-L-arginine methyl ester (L-NAME) did not attenuate the early phase of venom-induced hypotension, but abolished the recovery phase and resulted in rapid death; a similar effect was observed with the soluble guanylate cyclase (sGC) inhibitor ODQ. In contrast, the hemodynamic responses to venom were not attenuated by the non-selective NOS inhibitor N -monomethyl-L-arginine, the inducible NOS inhibitor aminoguanidine, the phosphodiesterase 5 inhibitor sildenafil, the adenylate cyclase (AC) inhibitor SQ-22.536, the non-selective muscarinic receptor antagonist atropine, the bradykinin B2 receptor antagonist HOE-140 and the non-selective cyclooxygenase inhibitor indomethacin. Preincubation of venom with the PLA inhibitor pBPB had no effect on the immediate hypotension but tended to improve the recovery phase. Neither AEBSF (a serine proteinase inhibitor) nor EDTA (a metalloproteinase inhibitor) prevented the venom-induced hypotension, but AEBSF and not EDTA protected against the lethality of a high dose (3.0 mg/kg, i.v.). There were no marked changes in the ECG parameters with the various treatments, except with L-NAME and ODQ that increased the RR interval. Pulmonary thrombus formation was markedly enhanced by L-NAME and ODQ, and to a lesser extent by pBPB, especially in small vessels, whereas AEBSF and EDTA inhibited thrombus formation. Venom relaxed phenylephrine-precontracted thoracic aorta and pulmonary artery in vitro, with the latter being more sensitive. The relaxation was endothelium-dependent and was inhibited by ODQ but not by H-89, a protein kinase A (PKA) inhibitor. Together, these findings indicate involvement of the NO/sGC/cGMP, but not the AC/cAMP/PKA signaling pathway, in the hemodynamic responses to L. muta venom in rats. Muscarinic mechanisms, kinins and arachidonic acid metabolites are apparently not involved.
[Mh] Termos MeSH primário: Hemodinâmica/efeitos dos fármacos
Venenos de Víboras/toxicidade
Viperidae
[Mh] Termos MeSH secundário: Animais
Aorta Torácica/efeitos dos fármacos
Inibidores Enzimáticos/uso terapêutico
Hipotensão/induzido quimicamente
Técnicas In Vitro
Cininas/metabolismo
Cininas/fisiologia
Masculino
NG-Nitroarginina Metil Éster/uso terapêutico
Sistema Nervoso Parassimpático/efeitos dos fármacos
Artéria Pulmonar/efeitos dos fármacos
Ratos Wistar
Transdução de Sinais
Mordeduras de Serpentes/tratamento farmacológico
Mordeduras de Serpentes/patologia
Mordeduras de Serpentes/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Kinins); 0 (Viper Venoms); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170518
[Lr] Data última revisão:
170518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE


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[PMID]:27486919
[Au] Autor:Guevara-Lora I; Niewiarowska-Sendo A; Polit A; Kozik A
[Ad] Endereço:Department of Analytical Biochemistry, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University in Krakow, Kraków, Poland.
[Ti] Título:Hypothetical orchestrated cooperation between dopaminergic and kinin receptors for the regulation of common functions.
[So] Source:Acta Biochim Pol;63(3):387-96, 2016.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:The G protein-coupled receptors (GPCRs), one of the largest protein families, are essential components of the most commonly used signal-transduction systems in cells. These receptors, often using common pathways, may cooperate in the regulation of signal transmission to the cell nucleus. Recent scientific interests increasingly focus on the cooperation between these receptors, particularly in a context of their oligomerization, e.g. the formation of dimers that are able to change characteristic signaling of each receptor. Numerous studies on kinin and dopamine receptors which belong to this family of receptors have shown new facts demonstrating their direct interactions with other GPCRs. In this review, current knowledge on signaling pathways and oligomerization of these receptors has been summarized. Owing to the fact that kinin and dopamine receptors are widely expressed in cell membranes where they act as mediators of numerous common physiological processes, the information presented here sheds new light on a putative crosstalk of these receptors and provides more comprehensive understanding of possible direct interactions that may change their functions. The determination of such interactions may be useful for the development of new targeted therapeutic strategies against many disorders in which kinin and dopamine receptors are involved.
[Mh] Termos MeSH primário: Receptores Dopaminérgicos/fisiologia
[Mh] Termos MeSH secundário: Animais
Dopamina/fisiologia
Seres Humanos
Cininas/fisiologia
Multimerização Proteica
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Kinins); 0 (Receptors, Dopamine); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170124
[Lr] Data última revisão:
170124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160804
[St] Status:MEDLINE
[do] DOI:10.18388/abp.2016_1366


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[PMID]:27468462
[Au] Autor:Agrawal N; Akella A; Deshpande SB
[Ti] Título:Captopril augments acetylcholine-induced bronchial smooth muscle contractions in vitro via kinin-dependent mechanisms.
[So] Source:Indian J Exp Biol;54(6):365-9, 2016 Jun.
[Is] ISSN:0019-5189
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:Angiotensin converting enzyme (ACE) inhibitors therapy is aassociated with bothersome dry cough as an adverse effect. The mechanisms underlying this adverse effect are not clear. Therefore, influence of captopril (an ACE inhibitor) on acetylcholine (ACh)-induced bronchial smooth muscle contractions was investigated. Further, the mechanisms underlying the captopril-induced changes were also explored. In vitro contractions of rat bronchial smooth muscle to cumulative concentrations of ACh were recorded before and after exposure to captopril. Further, the involvement of kinin and inositol triphosphate (IP3) pathways for captopril-induced alterations were explored. ACh produced concentration-dependent (5-500 µM) increase in bronchial smooth muscle contractions. Pre-treatment with captopril augmented the ACh-induced contractions at each concentration significantly. Pre-treatment with aprotinin (kinin synthesis inhibitor) or heparin (inositol triphosphate, IP3-inhibitor), blocked the captopril-induced augmentation of bronchial smooth muscle contractions evoked by ACh. Further, captopril-induced augmentation was absent in calcium-free medium. These results suggest that captopril sensitizes bronchial smooth muscles to ACh-induced contractions. This sensitization may be responsible for dry cough associated with captopril therapy.
[Mh] Termos MeSH primário: Acetilcolina/efeitos adversos
Inibidores da Enzima Conversora de Angiotensina/efeitos adversos
Brônquios/efeitos dos fármacos
Captopril/efeitos adversos
Contração Muscular/efeitos dos fármacos
Músculo Liso/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Espasmo Brônquico/induzido quimicamente
Tosse/induzido quimicamente
Sinergismo Farmacológico
Cininas/metabolismo
Masculino
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Kinins); 9G64RSX1XD (Captopril); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160729
[Lr] Data última revisão:
160729
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160730
[St] Status:MEDLINE


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[PMID]:27274056
[Au] Autor:Kwon H; Ali Agha M; Smith RC; Nachman RJ; Marion-Poll F; Pietrantonio PV
[Ad] Endereço:Department of Entomology, Texas A&M University, College Station, TX 77843;
[Ti] Título:Leucokinin mimetic elicits aversive behavior in mosquito Aedes aegypti (L.) and inhibits the sugar taste neuron.
[So] Source:Proc Natl Acad Sci U S A;113(25):6880-5, 2016 06 21.
[Is] ISSN:1091-6490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Insect kinins (leucokinins) are multifunctional peptides acting as neurohormones and neurotransmitters. In females of the mosquito vector Aedes aegypti (L.), aedeskinins are known to stimulate fluid secretion from the renal organs (Malpighian tubules) and hindgut contractions by activating a G protein-coupled kinin receptor designated "Aedae-KR." We used protease-resistant kinin analogs 1728, 1729, and 1460 to evaluate their effects on sucrose perception and feeding behavior. In no-choice feeding bioassays (capillary feeder and plate assays), the analog 1728, which contains α-amino isobutyric acid, inhibited females from feeding on sucrose. It further induced quick fly-away or walk-away behavior following contact with the tarsi and the mouthparts. Electrophysiological recordings from single long labellar sensilla of the proboscis demonstrated that mixing the analog 1728 at 1 mM with sucrose almost completely inhibited the detection of sucrose. Aedae-KR was immunolocalized in contact chemosensory neurons in prothoracic tarsi and in sensory neurons and accessory cells of long labellar sensilla in the distal labellum. Silencing Aedae-KR by RNAi significantly reduced gene expression and eliminated the feeding-aversion behavior resulting from contact with the analog 1728, thus directly implicating the Aedae-KR in the aversion response. To our knowledge, this is the first report that kinin analogs modulate sucrose perception in any insect. The aversion to feeding elicited by analog 1728 suggests that synthetic molecules targeting the mosquito Aedae-KR in the labellum and tarsi should be investigated for the potential to discover novel feeding deterrents of mosquito vectors.
[Mh] Termos MeSH primário: Aedes/fisiologia
Cininas/farmacologia
Mimetismo Molecular
Neurônios/fisiologia
Sacarose
Paladar
[Mh] Termos MeSH secundário: Animais
Clonagem Molecular
DNA Complementar
Feminino
Seres Humanos
Cininas/química
Masculino
Microscopia Confocal
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Kinins); 57-50-1 (Sucrose)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160609
[St] Status:MEDLINE
[do] DOI:10.1073/pnas.1520404113



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