Littérature scientifique sur le sujet « Renovascular disease »
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Articles de revues sur le sujet "Renovascular disease"
Kalra, Philip A. « Renovascular Disease ». Medicine 31, no 7 (juillet 2003) : 116–18. http://dx.doi.org/10.1383/medc.31.7.116.28477.
Texte intégralKalra, Philip A. « Renovascular disease ». Medicine 35, no 7 (juillet 2007) : 406–9. http://dx.doi.org/10.1016/j.mpmed.2007.04.003.
Texte intégralKalra, Philip A. « Renovascular disease ». Medicine 39, no 6 (juin 2011) : 364–68. http://dx.doi.org/10.1016/j.mpmed.2011.03.007.
Texte intégralVassallo, Diana, et Philip A. Kalra. « Renovascular disease ». Medicine 43, no 7 (juillet 2015) : 419–24. http://dx.doi.org/10.1016/j.mpmed.2015.04.008.
Texte intégralVassallo, Diana, et Philip A. Kalra. « Renovascular disease ». Medicine 47, no 8 (août 2019) : 526–32. http://dx.doi.org/10.1016/j.mpmed.2019.05.008.
Texte intégralRANKIN, SHEILA C., ANDREW J. S. SAUNDERS, GARY J. R. COOK et JOHN E. SCOBLE. « Renovascular Disease ». Clinical Radiology 55, no 1 (janvier 2000) : 1–12. http://dx.doi.org/10.1053/crad.1999.0338.
Texte intégralMatsumoto, Alan H. « Renovascular Disease ». Journal of Vascular and Interventional Radiology 14, no 2 (février 2003) : P60—P61. http://dx.doi.org/10.1016/s1051-0443(03)70089-x.
Texte intégralLibertino, John A. « Renovascular disease ». Current Opinion in Urology 3, no 2 (avril 1993) : 107–9. http://dx.doi.org/10.1097/00042307-199304000-00010.
Texte intégralHamilton, George. « Renovascular disease ». Current Opinion in Urology 4, no 2 (mars 1994) : U49. http://dx.doi.org/10.1097/00042307-199403000-00011.
Texte intégralOlin, Jeffrey W. « Atherosclerotic renovascular disease ». Current Opinion in Cardiology 5, no 5 (octobre 1990) : 659–65. http://dx.doi.org/10.1097/00001573-199010000-00016.
Texte intégralThèses sur le sujet "Renovascular disease"
Vassallo, Diana. « Atherosclerotic renovascular disease : risk prediction and selection for revascularization ». Thesis, University of Manchester, 2018. https://www.research.manchester.ac.uk/portal/en/theses/atherosclerotic-renovascular-disease-risk-prediction-and-selection-for-revascularization(ff841ec0-ae14-40a1-9865-dc014f977a77).html.
Texte intégralShurrab, Alaa Eldeen. « Relationship of parenchymal disease to renal dysfunction in patients with atherosclerotic renovascular disease ». Thesis, University of Manchester, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.492719.
Texte intégralRitchie, James. « Epidemiology of atherosclerotic renovascular disease : clinical presentations, prognosis and treatment ». Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/epidemiology-of-atherosclerotic-renovascular-disease-clinical-presentations-prognosis-and-treatment(c86ec7c6-a636-48b7-9f3e-c086b8cc4905).html.
Texte intégralCheung, Ching-Mei. « Evaluation of Renal Morphology, Function and Outcome in Atherosclerotic Renovascular Disease ». Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.509057.
Texte intégralMacêdo, Thiago Andrade de. « Estudo dos determinantes de doença arterial coronária grave em pacientes hipertensos com indicação de arteriografia renal por suspeita de estenose de artéria rena ». Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-11072012-094212/.
Texte intégralINTRODUCTION: In patients with suspected coronary artery disease (CAD), indications for performing coronary and renal angiography at the same setting are well established. However, in hypertensive patients with suspected renal artery stenosis (RAS) with indication for renal angiography, it is not well defined the determinants of the presence of severe CAD. OBJECTIVES: We aimed to evaluate the prevalence and determinants of severe CAD in hypertensive patients referred to renal angiography for the diagnosis of RAS. METHODS: Eighty-two consecutive patients with high clinical risk for RAS systematically underwent renal angiography and coronary angiography at the same procedure. Significant RAS and CAD were defined as arterial luminal obstruction 70%. RESULTS: Either significant RAS or significant CAD were present in 32/82 patients (39%). Patients with severe CAD were older (63±12 vs. 56±13 years, p=0.03), had more angina (41 vs. 16%; p=0.013), higher left atrial diameter (44.7 vs. 40,6mm; p=0.005), and higher pulse wave velocity (12.6 vs. 10.7 m/s); p=0.02) compared to patients without significant CAD. Significant RAS was associated with an increased prevalence of severe CAD compared to patients without the lesion (66% vs. 22%, respectively; p<0.001). Binary logistic regression analysis showed that RAS 70% was independently associated with severe CAD (OR: 11.48; 95%CI 3.2-40.2; p<0.001), even in patients without angina (OR: 13.48; 95%CI 2.6-12.1; p<0.001). CONCLUSION: The prevalence of severe CAD in hypertensive patients with significant RAS is high. The presence of RAS 70%, diagnosed by renal angiography, is a strong and useful predictor to identify severe CAD, independently of the presence of angina
Ramos, Filho Antonio Celso S. « Avaliação morfofuncional e molecular do detrusor isolado de ratos hipertensos renovasculares ». [s.n.], 2010. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308915.
Texte intégralDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-17T00:06:55Z (GMT). No. of bitstreams: 1 RamosFilho_AntonioCelsoS._M.pdf: 1693116 bytes, checksum: 4526088a65a406983163ece45558e71c (MD5) Previous issue date: 2010
Resumo: A hipertensão renovascular é uma forma secundária da hipertensão arterial, que corresponde de 1-5% dos casos de hipertensão. A associação entre hipertensão arterial e disfunções miccionais foi observada no modelo experimental de ratos espontaneamente hipertensos (SHR). Até o momento nenhum estudo avaliou as disfunções miccionais em animais hipertensos renovasculares. Dessa forma, neste estudo, caracterizamos a disfunção miccional em ratos hipertensos renovasculares através do modelo de dois rins, um clip (2K-1C). Em ratos Wistar (200-220 g) colocou-se um clip em torno da artéria renal. Depois de oito semanas, os ratos foram utilizados. Realizou-se estudo cistométrico em ratos anestesiados, assim como curvas concentração-resposta para agentes contráteis e relaxantes em detrusor isolado (DSM). Foram também realizados estudos histomorfométricos e da expressão de RNAm dos receptores muscarínicos M3 e M2 em DSM isolado. Os resultados histomorfométricos mostraram aumentos significantes na espessura da parede da bexiga, no volume intravesical, na densidade de musculatura lisa e na densidade de fibras neurais no grupo 2K-1C em comparação ao SHAM. O agonista muscarínico, carbacol, produziu contrações concentração-dependentes do DSM, as quais foram significantemente maiores no grupo 2K-1C. O inibidor da Rho-quinase, Y27-632 (10 µM), reduziu significantemente a contração induzida pelo carbacol nos ratos SHAM e 2K-1C; porém, no grupo 2K-1C, o DSM continuou hiperativo na presença do Y27-632. A estimulação elétrica (1 - 32 Hz) produziu contração freqüência-dependente do DSM as quais foram maiores no grupo 2K-1C. O agonista purinérgico P2X, ?,?-metileno-ATP (1 - 100 µM), o KCl (1 - 300 µM) e o Ca2+ extracelular (0,01-100 µM) produziram contrações concentração-dependente; porém, não observamos diferenças entre o grupo SHAM e 2K-1C. O agonista não seletivo ?-adrenérgico, isoproterenol, o agonista seletivo ?2-adrenérgico, metaproterenol, e o agonista seletivo ?3-adrenérgico, BRL37-344, produziram relaxamentos menores do DSM nos ratos 2K-1C, e também redução nos níveis intracelulares de AMPc nos detrusores. O efeito relaxante ao nitroprussiato de sódio e BAY41-2272 mantiveram-se iguais nos animais SHAM e 2K-1C. A expressão do RNAm do receptor muscarínico M3 (mas não do M2) no DSM foi significantemente maior nos ratos 2K-1C em comparação ao grupo controle. Os tratamentos crônicos com losartan e captopril normalizaram a pressão arterial sistólica dos animais 2K-1C, normalizaram a função miccional, e reduziram a hipercontratilidade do detrusor induzida pela estimulação elétrica e pelo carbacol, assim como restabeleceram o relaxamento induzido pelo isoproterenol ao nível do grupo SHAM. Concluimos que os ratos hipertensos renovasculares apresentam hiperatividade do detrusor, a qual envolve remodelamento tecidual e aumento da contração via receptor muscarínico M3 associado à redução no relaxamento ?-adrenérgico com redução da sinalização intracelular e produção de AMPc. Os tratamentos com losartan e captopril restauram a função miccional dos animais 2K-1C
Abstract: Renovascular hypertension is a secondary form of arterial hypertension, accounting for 1-5% of cases in unselected population. Association between arterial hypertension and urinary bladder dysfunction has been reported in spontaneously hypertensive rats, but no study evaluated the bladder dysfunction in renovascular hypertensive animals. Therefore, in this study, we explored the bladder dysfunction in renovascular hypertensive rats, using the two-kidney one-clip (2K-1C) model. A silver clip was placed around the renal artery of male Wistar Kyoto rats (200-220 g). After eight weeks, rats were used. Cystometric study in anesthetized rats, along with concentration-response curves to both contractile and relaxant agents in isolated detrusor smooth muscle (DSM) were performed. Histomorphometry and mRNA expression of muscarinic M3 and M2 receptors in DSM were also determined. The histomorphometric data showed significant increases in bladder wall thickness, intravesical volume and density of smooth muscle, as well as density of neural fibers in the 2K-1C group compared with SHAM. The muscarinic agonist carbachol produced concentration-dependent DSM contractions, which were markedly greater in 2K-1C rats. The Rho-kinase inhibitor Y27-632 (10 µM) significantly reduced the carbachol-induced contractions in sham and 2K-1C rats, but DSM in 2K-1C rats remained overactive in the presence of Y27632. Electrical-field stimulation (EFS; 1-32 Hz) produced frequency-dependent DSM contractions that were also greater in 2K-1C group. The P2X receptor agonist ?,?-methylene ATP (1-100 µM), KCl (1-300 mM) and extracellular Ca2+ (0.01-100 M) produced concentration-dependent DSM contractions, but no changes among sham and 2K-1C rats were seen. In 2K-1C rats, the non-selective ?-adrenoceptor agonist isoproterenol, the ?2-adrenoceptor agonist metaproterenol and the ?3-adrenoceptor agonist BRL 37-344 produced lower DSM relaxations, as well as decreased cAMP levels. The relaxant responses to sodium nitroprusside and BAY 41-2272 remained unchanged in 2K-1C rats. Expression of mRNA of muscarinic M3 (but not of M2) receptors in DSM was significantly increased in 2K-1C rats. The chronic treatment with losartan and captopril normalized the blood systolic pressure of 2K-1C animals, improved their urinary function by reducing DSM hypercontractility to EFS and carbacol stimulation, and restored the relaxation induced by the ?-adrenergic agonist isoproterenol to the level of SHAM group. In conclusion, renovascular hypertensive rats exhibit overactive DSM that involves tissue remodeling and enhanced muscarinic M3-mediated contractions associated with reduced ?-adrenoceptor-mediated signal transduction. The treatments with losartan and captopril improved urinary function of 2K-1C animals
Mestrado
Mestre em Farmacologia
Chen, Ying-Hsiang, et 陳瀅翔. « The Therapeutic and Preventive Effects of Sodium Thiosulfate in Chronic Kidney Disease and Renovascular Hypertension in Rats ». Thesis, 2019. http://ndltd.ncl.edu.tw/handle/a44r5x.
Texte intégralFAVA, Cristiano. « Metabolites of arachidonic acid via CYP450 in human hypertension ». Doctoral thesis, 2008. http://hdl.handle.net/11562/337636.
Texte intégralBackground: In the last years there has been considerable interest in exploring the role of 20- hydroxyeicosatetraenoic acid (20-HETE) and 5,6-, 8,9-, 11,12- and 14,15 epoxyeicosatrienoic acids (EETs), metabolites of arachidonic acid via cythochrome P450 (CYP), in hypertension, given the importance of this pathway in the regulation of renal and peripheral vascular tone and the renal handling of sodium. The CYP4A11 and the CYP4F2 are responsible for renal production of 20-HETE. The CYP4A11 F434S and CYP4F2 V433M polymorphisms reduce 20- HETE production, in vitro. Aims: The aim of the first study was to investigate whether activation of the renin angiotensin system in renovascular disease affects the CYP ω-ω-1 hydroxylase (20-HETE) and epoxygenase (EETs) pathways of arachidonic acid metabolism in vivo, each of which interacts with Angiotnsin II (study 1). The aim of the second study was to evaluate the effect of the mentioned polymorphisms on blood pressure (BP) levels, hypertension prevalence and cardiovascular events in a large cohort of middle-aged Swedes (study 2). Methods: Plasma concentration and urinary excretion of 20-HETE, and EETs and their metabolites, dihydroxyeicosatrienoic acids (DHETs), were measured in urine and plasma by mass spectrometry in 10 subjects with renovascular disease, 10 with essential hypertension, and 10 healthy normotensive subjects (controls), pair-matched for gender and age. Vascular and renal function was evaluated in all subjects (study 1). The polymorphisms were genotyped in the cardiovascular cohort of the Malmö Diet and Cancer (MDC-CVA) study. The incidence of fatal and non-fatal cardiovascular events (coronary events, n= 268, and ischemic stroke, n =194) was monitored over 10 years of follow-up. The analysis of blood pressure levels was performed twice: excluding subjects under antihypertensive treatment and including them (study 2). Results: Plasma 20-HETE was highest in subjects with renovascular disease [1.20 (0.42-1.92) ng/mL, median and range] compared to essential hypertensives [0.90 ng/mL (0.40-2.1)] and Metabolites of arachidonic acid via CYP450 in human hypertension controls [0.45 ng/mL (0.14-1.7), P<0.05]. Plasma 20- HETE significantly correlated with plasma renin activity (PRA) in renovascular disease (rs=0.67, n=10, P<0.05). The urinary excretion of 20-HETE was significantly lower in subjects with renovascular disease [12.9, (4.4-24.9) μg/g creatinine] than in controls [31.0 (11.9-102.8) μg/g creatinine, P<0.01)] and essential hypertensives [35.9 (14-72.5) μg/g creatinine, P<0.05]. Total plasma EETs were lowest as was the ratio of plasma EETs to plasma DHETs, an index of epoxide hydrolase activity, in renovascular disease [ratio 2.4 (1.2-6.1)], compared to essential hypertension [3.4 (1.5-5.6)] and controls [6.8 (1.4-18.8), P<0.01] (study 1). In the whole population, CYP4A11 S434S homozygotes had higher adjusted (for number of antihypertensive drugs) and non-adjusted systolic BP and higher prevalence of hypertension respect to F434 carriers. Male but not female CYP4F2 M433 carriers had significantly higher adjusted and non-adjusted systolic and diastolic BP and a trend toward higher hypertension prevalence (p=0.06) respect to V433V homozygotes. After adjustment for major cardiovascular risk factors, the hazard ratio (HR) for ischemic stroke in male CYP4F2 M433 carriers was significantly higher respect to V433V homozygotes (HR 1.69; 95%C.I. 1.1-2.6) even when BP levels and hypertension prevalence were included in the COX proportional-hazard model (study 2). Conclusion: circulating levels of 20-HETE are increased and those of EETs are decreased in RVD, while the urinary excretion of 20-HETE is reduced. Altered CYP 450 arachidonic acid metabolism may contribute to the vascular and tubular abnormalities of RVD (study 1). A common V433M polymorphism of the CYP4F2 might increase the risk of incident ischemic stroke in males but only partially through its elevating effect on BP. Further studies are needed to confirm these data (study 2).
Livres sur le sujet "Renovascular disease"
Renal Vascular Disease. W.B. Saunders Company, 1996.
Trouver le texte intégralKatritsis, Demosthenes G., Bernard J. Gersh et A. John Camm. Secondary hypertension. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199685288.003.0502_update_002.
Texte intégralRitchie, James, Darren Green, Constantina Chrysochou et Philip A. Kalra. Renal artery stenosis. Sous la direction de Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0213.
Texte intégralAlderson, Helen, Constantina Chrysochou, James Ritchie et Philip A. Kalra. Ischaemic nephropathy. Sous la direction de Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0212.
Texte intégralJolly, Elaine, Andrew Fry et Afzal Chaudhry, dir. Renal medicine. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199230457.003.0017.
Texte intégralSalama, Alan D. The patient with vasculitis. Sous la direction de Giuseppe Remuzzi. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0159_update_001.
Texte intégralRitchie, James, Darren Green, Constantina Chrysochou et Philip A. Kalra. Renal artery stenosis. Sous la direction de Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0215.
Texte intégralRitchie, James, Darren Green, Constantina Chrysochou et Philip A. Kalra. Renal artery stenosis. Sous la direction de Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0214.
Texte intégralAlchi, Bassam, et David Jayne. The patient with antiphospholipid syndrome with or without lupus. Sous la direction de Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.
Texte intégralChapitres de livres sur le sujet "Renovascular disease"
Findlay, Mark, et Christopher Isles. « Renovascular Disease ». Dans Clinical Companion in Nephrology, 119–22. Cham : Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14868-7_23.
Texte intégralKirksey, Lee. « Renovascular Disease ». Dans Cleveland Clinic Manual of Vascular Surgery, 69–78. New York, NY : Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1631-3_6.
Texte intégralBien, Christian G., Christian E. Elger, Ali R. Afzal, Sirajedin Natah, Ritva Häyrinen-Immonen, Yrjö Konttinen, George S. Zubenko et al. « Renovascular Disease ». Dans Encyclopedia of Molecular Mechanisms of Disease, 1830. Berlin, Heidelberg : Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6710.
Texte intégralde Leeuw, Peter W., et Costas Tsioufis. « Atherosclerotic Renovascular Disease ». Dans Secondary Hypertension, 21–32. Cham : Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45562-0_2.
Texte intégralBien, Christian G., Christian E. Elger, Ali R. Afzal, Sirajedin Natah, Ritva Häyrinen-Immonen, Yrjö Konttinen, George S. Zubenko et al. « Renovascular Hypertension ». Dans Encyclopedia of Molecular Mechanisms of Disease, 1830. Berlin, Heidelberg : Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6712.
Texte intégralZhang, Xin, et Alfonso Eirin. « Models of Renovascular Disease ». Dans Renal Vascular Disease, 105–16. London : Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-2810-6_6.
Texte intégralVaughan, E. Darracott, Thomas G. Pickering, David B. Case, Thomas A. Sos et John H. Laragh. « Hypertension in Renovascular Disease ». Dans Hypertension in Kidney Disease, 77–98. Dordrecht : Springer Netherlands, 1986. http://dx.doi.org/10.1007/978-94-009-4271-4_4.
Texte intégralCanzanello, Vincent J. « Medical Management of Renovascular Disease ». Dans Renal Vascular Disease, 305–16. London : Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-2810-6_19.
Texte intégralNagaratnam, Nages, Kujan Nagaratnam et Gary Cheuk. « Renovascular Disease in the Elderly ». Dans Geriatric Diseases, 1–4. Cham : Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-32700-6_35-1.
Texte intégralNagaratnam, Nages, Kujan Nagaratnam et Gary Cheuk. « Renovascular Disease in the Elderly ». Dans Geriatric Diseases, 273–76. Cham : Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-33434-9_35.
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