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Alternative pathways for angiotensin II generation in the cardiovascular system

BECARI, C.; OLIVEIRA, E.B.; SALGADO, M.C.O.
Fonte: Associação Brasileira de Divulgação Científica Publicador: Associação Brasileira de Divulgação Científica
Tipo: Artigo de Revista Científica
ENG
Relevância na Pesquisa
66.39%
The classical renin-angiotensin system (RAS) consists of enzymes and peptides that regulate blood pressure and electrolyte and fluid homeostasis. Angiotensin II (Ang II) is one of the most important and extensively studied components of the RAS. The beneficial effects of angiotensin converting enzyme (ACE) inhibitors in the treatment of hypertension and heart failure, among other diseases, are well known. However, it has been reported that patients chronically treated with effective doses of these inhibitors do not show suppression of Ang II formation, suggesting the involvement of pathways alternative to ACE in the generation of Ang II. Moreover, the finding that the concentration of Ang II is preserved in the kidney, heart and lungs of mice with an ACE deletion indicates the important role of alternative pathways under basal conditions to maintain the levels of Ang II. Our group has characterized the serine protease elastase-2 as an alternative pathway for Ang II generation from Ang I in rats. A role for elastase-2 in the cardiovascular system was suggested by studies performed in heart and conductance and resistance vessels of normotensive and spontaneously hypertensive rats. This mini-review will highlight the pharmacological aspects of the RAS...

Adição de Bloqueador do receptor de angiotensina II na insuficiência cardíaca descompensada; Angiotensin II receptor blocker add-on therapy for low cardiac output in decompensated heart failure; Adición de bloqueante del receptor de angiotensina II en la insuficiencia cardiaca descompensada

OCHIAI, Marcelo E.; BARRETTO, Antonio C. P.; CARDOSO, Juliano N.; MUNHOZ, Robinson T.; MORGADO, Paulo C.; RAMIRES, José A. F.
Fonte: Sociedade Brasileira de Cardiologia - SBC Publicador: Sociedade Brasileira de Cardiologia - SBC
Tipo: Artigo de Revista Científica
POR
Relevância na Pesquisa
66.39%
FUNDAMENTO: Durante a descompensação da insuficiência cardíaca, ocorre uma intensa ativação do sistema renina-angiotensina-aldosterona, entretanto, o uso de inibidor da enzima de conversão de angiotensina (IECA) não pode bloqueá-lo completamente. De outro modo, a adição de bloqueador do receptor de angiotensina II (BRA) pode ser útil quando ocorre a dependência de inotrópico. Avaliamos a eficiência da associação BRA-IECA para retirada da dobutamina na insuficiência cardíaca avançada e descompensada. OBJETIVO: Avaliar a eficácia da associação de bloqueador do receptor AT1 de angiotensina II ao inibidor de enzima de conversão, para a retirada da dobutamina em pacientes com dependência de suporte inotrópico decorrente da descompensação aguda da insuficiência cardíaca crônica. MÉTODOS: Em um estudo caso-controle (N = 24), selecionamos pacientes internados por descompensação da insuficiência cardíaca e com uso por mais de 15 dias de dobutamina, ou uma ou mais tentativas sem sucesso de retirada; dose otimizada de IECA; e FEVE < 0,45. Os pacientes então receberam adicionalmente BRA (n = 12) ou não (controle, n = 12). O desfecho foi o sucesso na retirada da dobutamina, avaliado pela regressão logística...

Involvement of the AT(1) receptor in the venoconstriction induced by angiotensin II in both the inferior vena cava and femoral vein

SILVA, Osmar Gomes da; ROSSIGNOLI, Patricia de Souza; CARRILLO-SEPULVEDA, Maria Alicia; BARRETO-CHAVES, Maria Luiza Morais; CHIES, Agnaldo Bruno
Fonte: ELSEVIER SCIENCE INC Publicador: ELSEVIER SCIENCE INC
Tipo: Artigo de Revista Científica
ENG
Relevância na Pesquisa
66.42%
Although angiotensin II-induced venoconstriction has been demonstrated in the rat vena cava and femoral vein, the angiotensin II receptor subtypes (AT(1) or AT(2)) that mediate this phenomenon have not been precisely characterized. Therefore, the present study aimed to characterize the pharmacological receptors involved in the angiotensin II-induced constriction of rat venae cavae and femoral veins, as well as the opposing effects exerted by locally produced prostanoids and NO upon induction of these vasomotor responses. The obtained results suggest that both AT(1) and AT(2) angiotensin II receptors are expressed in both veins. Angiotensin II concentration-response curves were shifted toward the right by losartan but not by PD 123319 in both the vena cava and femoral vein. Moreover, it was observed that both 10(-5) M indomethacin and 10(-4) M L-NAME improve the angiotensin II responses in the vena cava and femoral vein. In conclusion, in the rat vena cava and femoral vein, angiotensin II stimulates AT(1) but not AT(2) to induce venoconstriction, which is blunted by vasodilator prostanoids and NO. (C) 2010 Elsevier Inc. All rights reserved.; Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)[05/51550-4]; Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

The role of reactive oxygen species in the modulation of the contraction induced by angiotensin II in carotid artery from diabetic rat

Pernomian, Larissa; Gomes, Mayara Santos; Araujo Restini, Carolina Baraldi; Zambelli Ramalho, Leandra Naira; Tirapelli, Carlos Renato; Oliveira, Ana Maria de
Fonte: ELSEVIER SCIENCE BV; AMSTERDAM Publicador: ELSEVIER SCIENCE BV; AMSTERDAM
Tipo: Artigo de Revista Científica
ENG
Relevância na Pesquisa
66.45%
The modulation played by reactive oxygen species on the angiotensin II-induced contraction in type I-diabetic rat carotid was investigated. Concentration-response curves for angiotensin II were obtained in endothelium-intact or endothelium-denuded carotid from control or streptozotocin-induced diabetic rats, pre-treated with tiron (superoxide scavenger), PEG-catalase (hydrogen peroxide scavenger), dimethylthiourea (hydroxyl scavenger), apocynin [NAD(P) H oxidase inhibitor], SC560 (cyclooxygenase-1 inhibitor), SC236 (cyclooxygenase-2 inhibitor) or Y-27632 (Rho-kinase inhibitor). Reactive oxygen species were measured by flow cytometry in dihydroethidium (DHE)-loaded endothelial cells. Cyclooxygenase and AT1-receptor expression was assessed by immunohistochemistry. Diabetes increased the angiotensin II-induced contraction but reduced the agonist potency in rat carotid. Endothelium removal, tiron or apocynin restored the angiotensin II-induced contraction in diabetic rat carotid to control levels. PEG-catalase, DMTU or SC560 reduced the angiotensin II-induced contraction in diabetic rat carotid at the same extent. SC236 restored the angiotensin II potency in diabetic rat carotid. Y-27632 reduced the angiotensin II-induced contraction in endothelium-intact or -denuded diabetic rat carotid. Diabetes increased the DHE-fluorescence of carotid endothelial cells. Apocynin reduced the DHE-fluorescence of endothelial cells from diabetic rat carotid to control levels. Diabetes increased the muscular cyclooxygenase-2 expression but reduced the muscular AT1-receptor expression in rat carotid. In summary...

Indução de receptor B1 de cininas em vasos sanguineos de ratos hipertensos por infusão de angiotensina II: estudo molecular e funcional.; Induction of kinin B1 receptor in blood vessels of angiotensin II-hypertensive rats: molecular and functional studies

Giaquinto, Luciana dos Reis Rigueiral
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Dissertação de Mestrado Formato: application/pdf
Publicado em 28/04/2011 PT
Relevância na Pesquisa
66.37%
O objetivo deste estudo foi avaliar se a infusão de angiotensina II (ANG II) modulava a expressão do receptor B1 (RB1) de cininas em aorta (AO),arteríolas mesentéricas (AM) de ratos Wistar e também verificar a influência do RB1 na pressão arterial e reatividade desses vasos sanguíneos através do agonista de RB1, DABK. Os ratos receberam por 28 dias infusão de ANG II ou de ANG II e antagonista de RB1. O DABK induziu relaxamento dependente de endotélio e NO em anéis de AO de ratos ANG II. A infusão de ANG II causou hipertensão arterial, aumento da expressão de RNAm de RB1 em AO e AM, da expressão protéica de RB1 em AO e disfunção endotelial caracterizada por diminuída resposta á acetilcolina (ACH).O antagonista de B1R não interferiu no desenvolvimento de hipertensão e na disfunção endotelial causada, mas aumentou a sensibilidade da AO à ACH e a expressão de NO Sintase nos ratos ANG II. Esses resultados nos permitem sugerir que a ANG II e cininas podem atuar sinergicamente no desenvolvimento das alterações vasculares observadas nesse modelo de hipertensão arterial.; The aim of the present study was to evaluate whether the angiotensin II (ANG II) infusion modulates the kinin B1 receptor (B1R) mRNA, protein expression in aorta (AO) and mesenteric arterioles (MA) in Wistar rats. It was also verified the role of RB1 in the control of blood pressure and vascular reactivity using DABK a B1R agonist Rats were infused either with ANG II (400ng/Kg/min) or ANG II plus RB1antagonist(350ng/Kg/min) during 28 days.DABK induced endothelium-NO dependent relaxation in AO of ANG II rats. ANG II infusion caused hypertension...

Conseqüências do estresse crônico ou agudo sobre as ações vasculares do Angiotensia II e da Angiotensina 1-7 em carótidas de ratos; Consequences of acute or chronic stress on the vascular actions of angiotensin II and angiotensin 1-7 in the rat carotid artery.

Banin, Tamy Midori
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Dissertação de Mestrado Formato: application/pdf
Publicado em 17/06/2011 PT
Relevância na Pesquisa
66.42%
O estresse crônico ou agudo pode alterar diversas funções relacionadas ao sistema cardiovascular, ocasionando doenças cardíacas. O sistema renina-angiotensina (SRA), importante participante do controle dessas funções, é profundamente afetado em resposta ao estresse. A angiotensina II (Ang II) é reconhecida como hormônio multifuncional que influencia diversos processos celulares importantes para a regulação da função vascular, incluindo regulação do tônus vascular, crescimento celular, dentre outros. Outro componente do SRA é a angiotensina 1-7 (Ang 1-7), suas ações vasculares envolvem aumento na produção de prostanóides vasodilatadores, óxido nítrico e fator hiperpolarizante derivado do endotélio. O objetivo do presente trabalho foi avaliar as conseqüências do estresse, agudo ou crônico, sobre as atividades vasomotoras da Ang II e da Ang 1-7, os mecanismos envolvidos na contração e relaxamento induzidos, respectivamente, por estes peptídeos e as modificações na expressão dos receptores AT1, AT2 e Mas, em carótida de ratos. O estresse crônico levou à diminuição do ganho de peso corpóreo dos animais, promoveu remodelamento das artérias carótidas, com significativo aumento da camada média acompanhada de redução da resposta de relaxamento da Ang 1-7...

Angiotensina II e treinamento físico na insuficiência cardíaca: implicações para a miopatia esquelética; Angiotensin II and exercise training in Heart Failure: implications to skeletal muscle myopathy

Gomes-Santos, Igor Lucas
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Tese de Doutorado Formato: application/pdf
Publicado em 31/01/2014 PT
Relevância na Pesquisa
66.37%
INTRODUÇÃO: Capítulo 1. A Insuficiência Cardíaca (IC) é acompanhada de uma hiperativação simpática e do sistema renina-angiotensina (SRA). As ações deletérias do SRA são atribuídas à Angiotensina II (AngII), mas a Angiotensina-(1- 7) (Ang-(1-7)), um metabólito da AngII, demonstra efeitos cardiovasculares benéficos, contrários aos da AngII. O conceito tradicional é de que as concentrações sistêmicas mediam as respostas do SRA, mas evidências emergem acerca da importância funcional do SRA local. Nesse estudo, estudou-se o SRA circulante e muscular esquelético na IC, testando-se a hipótese de que as alterações seriam diferentes nesses dois territórios, e que o treinamento físico corrigiria essas alterações. Capítulo 2. A IC é uma síndrome sistêmica, onde fatores neuroendócrinos, como a AngII, podem levar a alterações periféricas. Na musculatura esquelética, a hiperatividade do sistema ubiquitina-proteassoma (SUP) é um dos elementos que compõem um quadro de miopatia, aumentando o catabolismo muscular em direção à atrofia, e contribuindo com o agravamento da síndrome. O treinamento físico normaliza o SUP e reduz as concentrações plasmáticas de AngII na IC. Dessa forma, testamos a hipótese de que a redução do SUP mediada pelo treinamento físico na IC depende da queda das concentrações plasmáticas de AngII. MÉTODOS: Capítulo 1. Ratos Wistar...

Estudo da participação da angiotensina II nas disfunções cardiovasculares induzidas pelo consumo crônico de etanol; Study of participation of angiotensin II in cardiovascular dysfunction induced by chronic ethanol consumption

Passaglia, Patrícia
Fonte: Biblioteca Digitais de Teses e Dissertações da USP Publicador: Biblioteca Digitais de Teses e Dissertações da USP
Tipo: Dissertação de Mestrado Formato: application/pdf
Publicado em 11/03/2014 PT
Relevância na Pesquisa
66.39%
A disfunção cardiovascular induzida pelo consumo crônico de etanol esta associada à formação de espécies reativas de oxigênio (ERO). A angiotensina II, via receptores AT1, é um importante formador de ERO no sistema cardiovascular. O objetivo foi avaliar a participação dos receptores AT1 nas disfunções cardiovasculares induzidas pelo consumo crônico de etanol. Ratos Wistar foram divididos em quatro grupos: Controle: recebeu água "ad libitum"; Etanol: recebeu solução de etanol 20% (vol./vol.); Controle+Losartan: recebeu água "ad libitum" e losartan (10 mg/kg) diariamente por gavagem; Etanol+Losartan: recebeu solução de etanol 20% e losartan. Foram realizadas aferições semanais da pressão arterial e freqüência cardíaca dos animais. Foram realizadas as dosagens para determinar: o nível de etanol no sangue; os níveis plasmáticos e teciduais (aorta e leito arterial mesentérico) de angiotensina I (ANG I) e ANG II; a atividade plasmática da renina; atividade plasmática e tecidual da enzima conversora de angiotensina (ECA); níveis plasmáticos de aldosterona; níveis plasmáticos do peptídeo natriurético atrial (ANP), vasopressina (AVP) e ocitocina (OT); a osmolaridade e o sódio plasmático; nitrato plasmático e tecidual; espécies reativas ao ácido tiobarbitútico (TBARS); a formação tecidual de ânion superóxido; a capacidade antioxidante total; além de verificar a expressão gênica e protéica (aorta) da via das MAPKs...

THE ROLE OF ANGIOTENSIN AT1 RECEPTORS IN THE DIURETIC, NATRIURETIC, KALIURETIC AND BLOOD-PRESSURE RESPONSES INDUCED BY ANGIOTENSIN-II ACTIVATION OF THE MEDIAN PREOPTIC NUCLEUS IN CONSCIOUS RATS

Ferreiradovale, C.; Renzi, A.; Camargo, GPA; Saad, W. A.; Luiz, A. C.; Menani, Jose Vanderlei; Silveira, JEN; Camargo, LAA
Fonte: Associação Brasileira de Divulgação Científica (ABRADIC) Publicador: Associação Brasileira de Divulgação Científica (ABRADIC)
Tipo: Artigo de Revista Científica Formato: 1097-1101
ENG
Relevância na Pesquisa
66.37%
We determined the effects of two classical angiotensin II (ANG II) antagonists, [Sar(1), Ala(8)]-ANG II and [Sar(1), Thr(8)]-ANG II, and losartan (a nonpeptide and selective antagonist for the AT 1 angiotensin receptors) on diuresis, natriuresis, kaliuresis and arterial blood pressure induced by ANG II administration into the median preoptic nucleus (MnPO) of male Holtzman rats weighing 250-300 g. Urine was collected in rats submitted to a water load (5% body weight) by gastric gavage, followed by a second water load (5% body weight) 1 h later. The volume of the drug solutions injected was 0.5 mu l over 10-15 s. Pre-treatment with [Sar(1), Ala(8)]-ANG II (12 rats) and [Sar(1), Thr(8)]-ANG II (9 rats), at the dose of 60 ng reduced (13.7 +/- 1.0 vs 11.0 +/- 1.0 and 10.7 +/- 1.2, respectively), whereas losartan (14 rats) at the dose of 160 ng totally blocked (13.7 +/- 1.0 vs 7.6 +/- 1.5) the urine excretion induced by injection of 12 ng of ANG II (14 rats). [Sar(1), Ala(8)]-ANG II impaired Na+ excretion (193 +/- 16 vs 120 +/- 19): whereas [Sar(1), Thr(8)]-ANG II and losartan blocked Na+ excretion (193 +/- 16 vs 77 +/- 15 and 100 +/- 12, respectively) induced by ANG II. Similar effects induced by ANG II on K+ excretion were observed with [Sar(1)...

Renal effects of angiotensin II receptor subtype 1 and 2-selective ligands injected into the paraventricular nucleus of conscious rats

Camargo, Luiz Antonio de Arruda; Saad, Wilson Abrão
Fonte: Universidade Estadual Paulista Publicador: Universidade Estadual Paulista
Tipo: Artigo de Revista Científica Formato: 91-96
ENG
Relevância na Pesquisa
66.37%
We determined the effects of losartan and CGP42112A (selective ligands of the AT1 and AT2 angiotensin receptors, respectively) and salarasin (a relatively nonselective angiotensin receptor antagonist) on urinary volume and urinary sodium and potassium excretion induced by administration of angiotensin II (ANG II) into the paraventricular nucleus (PVN) of conscious rats. Both the AT1 and AT2 ligands and salarasin administered in the presence of ANG II elicited a concentration-dependent inhibition of urine excretion, but losartan inhibited only 75% of this response. The IC50 for salarasin, CGP42112A, and losartan was 0.01, 0.05, and 6 nM, respectively. Previous treatment with saralasin, CGP42112A and losartan competitively antagonized the natriuretic responses to PVN administration of ANG II, and the IC50 values were 0.09, 0.48, and 10 nM, respectively. The maximum response to losartan was 65% of that obtained with saralasin. Pretreatment with saralasin, losartan, and CGP42112A injected into the PVN caused shifts to the right of the concentration-response curves, but the losartan concentrations were disproportionately greater compared with salarasin or CGP42112A. The IC50 values were 0.06, 0.5, and 7.0 for salarasin, CGP42112A, and losartan...

Influence of angiotensin II receptor subtypes of the paraventricular nucleus on the physiological responses induced by angiotensin II injection into the medial septal area

Saad, Wilson Abrão; De Arruda Camargo, Luiz Antonio
Fonte: Universidade Estadual Paulista Publicador: Universidade Estadual Paulista
Tipo: Artigo de Revista Científica Formato: 401-405
ENG
Relevância na Pesquisa
66.43%
Objective - We determined the effects of losartan and PD 123319 (antagonists of the AT1 and AT2 angiotensin receptors, respectively), and [Sar1, Ala8] ANG II (a relatively peptide antagonist of angiotensin receptors) injected into the paraventricular nucleus (PVN) on water and 3% NaCl intake, and the diuretic, natriuretic, and pressor effects induced by administration of angiotensin II (ANG II) into the medial septal area (MSA) of conscious rats. Methods - Holtzman rats were used. Animals were anesthetized with tribromoethanol (20 mg) per 100 grams of body weight, ip. A stainless steel guide cannula was implanted into the MSA and PVN. All drugs were injected in 0.5-μl volumes for 10-15 seconds. Seven days after brain surgery, water and 3% NaCl intake, urine and sodium excretion, and arterial blood pressure were measured. Results - Losartan (40 nmol) and [Sar1, Ala8] ANG II (40 nmol) completely eliminated whereas PD 123319 (40 nmol) partially blocked the increase in water and sodium intake and the increase in arterial blood pressure induced by ANG II (10 nmol) injected into the MSA. The PVN administration of PD 123319 and [Sar1, Ala8] ANG II blocked whereas losartan attenuated the diuresis and natriuresis induced by MSA administration of ANG II. Conclusion - MSA involvement with PVN on water and sodium homeostasis and arterial pressure modulation utilizing ANGII receptors is suggested.

Endothelial and neuronal nitric oxide synthase inhibitors influences angiotensin II pressor effect in central nervous system

Saad, Wilson Abrão; Guarda, Ismael Francisco Motta Siqueira; Camargo, Luiz Antonio de Arreda; Saad, William Abrão; Guarda, Renata Saad; Santos, A. F. B. Talmir; Simões, Sylvio
Fonte: Universidade Estadual Paulista Publicador: Universidade Estadual Paulista
Tipo: Artigo de Revista Científica Formato: 341-347
ENG
Relevância na Pesquisa
66.45%
The present study investigated the central role of angiotensin II and nitric oxide on arterial blood pressure (MAP) in rats. Losartan and PD123349 AT 1 and AT 2 (selective no peptides antagonists angiotensin receptors), as well as FK 409 (a nitric oxide donor), N W-nitro-L-arginine methyl ester (L-NAME) a constituve nitric oxide synthase inhibitor endothelial (eNOSI) and 7-nitroindazol (7NI) a specific neuronal nitric oxide synthase inhibitor (nNOSI) were used. Holtzman strain, (Rattus norvergicus) weighting 200-250 g were anesthetized with zoletil 50 mg kg -1 (tiletamine chloridrate 125 mg and zolazepan chloridrate 125 mg) into quadriceps muscle anda stainless steel cannula was stereotaxically implanted into their Lateral Ventricle (LV). Controls were injected with a 0.5 μl volume of 0.15 M NaCl. Angiotensin II injected into LV increased MAP (19±3 vs. control 3±1 mm Hg), which is potentiated by prior injection of L-NAME in the same site 26±2 mm Hg. 7NI injected prior to ANG II into LV also potentiated the pressor effect of ANG II but with a higher intensity than L-NAME 32±3 mm Hg. FK 409 inhibited the pressor effect of ANG II (6±1 mm Hg). Losartan injected into LV before ANG II influences the pressor effect of ANG II (8±1 mm Hg). The PD 123319 decreased the pressor effects of ANG II (16±1 mm Hg). Losartan injected simultaneously with FK 409 blocked the pressor effect of ANG II (3±1 mm Hg). L-NAME produced an increase in the pressor effect of ANG II...

Increased Expression of Angiotensin II Type 2 Receptors in the Solitary-Vagal Complex Blunts Renovascular Hypertension

Blanch, Graziela Torres; Freiria-Oliveira, Andre Henrique; Fina Speretta, Guilherme Fleury; Carrera, Eduardo J.; Li, Hongwei; Speth, Robert C.; Colombari, Eduardo; Sumners, Colin; Colombari, Debora S. A.
Fonte: Lippincott Williams & Wilkins Publicador: Lippincott Williams & Wilkins
Tipo: Artigo de Revista Científica Formato: 777-+
ENG
Relevância na Pesquisa
66.36%
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq); Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP); Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES); Processo FAPESP: 11/50770-1; Processo FAPESP: 13/50121-9; Angiotensin II increases and decreases arterial pressure by acting at angiotensin type 1 and type 2 receptors, respectively. Renovascular hypertensive rats exhibit a high level of activity of the peripheral and central renin-angiotensin system. Therefore, in the present study, we evaluated the effect of increasing the expression of angiotensin type 2 receptors in the solitary-vagal complex (nucleus of the solitary tract/dorsal motor nucleus of the vagus), a key brain stem region for cardiovascular regulation, on the development of renovascular hypertension. Holtzman normotensive rats were implanted with a silver clip around the left renal artery to induce 2-kidney 1-clip renovascular hypertension. Three weeks later, rats were microinjected in the solitary-vagal complex with either an adenoassociated virus to increase the expression of angiotensin type 2 receptors or with a control vector. We observed that increasing angiotensin type 2 receptor expression in the solitary-vagal complex attenuated the development of renovascular hypertension and also reversed the impairment of the baroreflex and the increase in the low-frequency component of systolic blood pressure observed in renovascular hypertensive rats. Furthermore...

Role of endothelium in angiotensin II formation by the rat aorta and mesenteric arterial bed

Fonte: Associação Brasileira de Divulgação Científica Publicador: Associação Brasileira de Divulgação Científica
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/05/1997 EN
Relevância na Pesquisa
66.42%
We investigated the angiotensin II (Ang II)-generating system by analyzing the vasoconstrictor effect of Ang II, angiotensin I (Ang I), and tetradecapeptide (TDP) renin substrate in the absence and presence of inhibitors of the renin-angiotensin system in isolated rat aortic rings and mesenteric arterial beds with and without functional endothelium. Ang II, Ang I, and TDP elicited a dose-dependent vasoconstrictor effect in both vascular preparations that was completely blocked by the Ang II receptor antagonist saralasin (50 nM). The angiotensin converting enzyme (ACE) inhibitor captopril (36 µM) completely inhibited the vasoconstrictor effect elicited by Ang I and TDP in aortic rings without affecting that of Ang II. In contrast, captopril (36 µM) significantly reduced (80-90%) the response to bolus injection of Ang I, without affecting those to Ang II and TDP in mesenteric arteries. Mechanical removal of the endothelium greatly potentiated (70-95%) the vasoconstrictor response to Ang II, Ang I, and TDP in aortic rings while these responses were unaffected by the removal of the endothelium of mesenteric arteries with sodium deoxycholate infusion. In addition, endothelium disruption did not change the pattern of response elicited by these peptides in the presence of captopril. These findings indicate that the endothelium may not be essential for Ang II formation in rat mesenteric arteries and aorta...

The hyperglycemia induced by angiotensin II in rats is mediated by AT1 receptors

Machado,L.J.C.; Marubayashi,U.; Reis,A.M.; Coimbra,C.C.
Fonte: Associação Brasileira de Divulgação Científica Publicador: Associação Brasileira de Divulgação Científica
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/10/1998 EN
Relevância na Pesquisa
66.48%
We have shown that the renin-angiotensin system (RAS) is involved in glucose homeostasis during acute hemorrhage. Since almost all of the physiological actions described for angiotensin II were mediated by AT1 receptors, the present experiments were designed to determine the participation of AT1 receptors in the hyperglycemic action of angiotensin II in freely moving rats. The animals were divided into two experimental groups: 1) animals submitted to intravenous administration of angiotensin II (0.96 nmol/100 g body weight) which caused a rapid increase in plasma glucose reaching the highest values at 5 min after the injection (33% of the initial values, P<0.01), and 2) animals submitted to intravenous administration of DuP-753 (losartan), a non-peptide antagonist of angiotensin II with AT1-receptor type specificity (1.63 µmol/100 g body weight as a bolus, iv, plus a 30-min infusion of 0.018 µmol 100 g body weight-1 min-1 before the injection of angiotensin II), which completely blocked the hyperglycemic response to angiotensin II (P<0.01). This inhibitory effect on glycemia was already demonstrable 5 min (8.9 ± 0.28 mM, angiotensin II, N = 9 vs 6.4 ± 0.22 mM, losartan plus angiotensin II, N = 11) after angiotensin II injection and persisted throughout the 30-min experiment. Controls were treated with the same volume of saline solution (0.15 M NaCl). These data demonstrate that the angiotensin II receptors involved in the direct and indirect hyperglycemic actions of angiotensin II are mainly of the AT1-type.

Alternative pathways for angiotensin II generation in the cardiovascular system

Becari,C.; Oliveira,E.B.; Salgado,M.C.O.
Fonte: Associação Brasileira de Divulgação Científica Publicador: Associação Brasileira de Divulgação Científica
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/09/2011 EN
Relevância na Pesquisa
66.39%
The classical renin-angiotensin system (RAS) consists of enzymes and peptides that regulate blood pressure and electrolyte and fluid homeostasis. Angiotensin II (Ang II) is one of the most important and extensively studied components of the RAS. The beneficial effects of angiotensin converting enzyme (ACE) inhibitors in the treatment of hypertension and heart failure, among other diseases, are well known. However, it has been reported that patients chronically treated with effective doses of these inhibitors do not show suppression of Ang II formation, suggesting the involvement of pathways alternative to ACE in the generation of Ang II. Moreover, the finding that the concentration of Ang II is preserved in the kidney, heart and lungs of mice with an ACE deletion indicates the important role of alternative pathways under basal conditions to maintain the levels of Ang II. Our group has characterized the serine protease elastase-2 as an alternative pathway for Ang II generation from Ang I in rats. A role for elastase-2 in the cardiovascular system was suggested by studies performed in heart and conductance and resistance vessels of normotensive and spontaneously hypertensive rats. This mini-review will highlight the pharmacological aspects of the RAS...

The effect of losartan on angiotensin II-induced cell proliferation in a rat aorta smooth muscle cell line

Tambelline,Natália; Oliveira,Karen; Olchanheski Junior,Luiz Renato; Sordi,Regina; Otuki,Michel Fleith; Favero,Giovani Marino; Fernandes,Daniel
Fonte: Instituto de Tecnologia do Paraná - Tecpar Publicador: Instituto de Tecnologia do Paraná - Tecpar
Tipo: Artigo de Revista Científica Formato: text/html
Publicado em 01/04/2012 EN
Relevância na Pesquisa
66.38%
The success of revascularization procedures is limited by recurrent stenosis, which is a narrowing of a blood vessels that results from neo-intimal hyperplasia. The renin-angiotensin-aldosterone system has been implicated in the pathogenesis of neo-intimal hyperplasia, and a role for angiotensin II in vascular smooth muscle cell proliferation has been proposed. There are at least two high-affinity subtypes of angiotensin II receptors, AT1 and AT2, both of which are seven-transmembrane G protein-coupled receptors. We investigated the effect of losartan, an AT1 receptor antagonist, on vascular smooth muscle cell proliferation using the A7r5 smooth cell line derived from rat aorta. Losartan was shown to prevent angiotensin II-induced cell proliferation, thereby suggesting that the effect of angiotensin II was mediated via AT1 receptors. These data strengthen the concept that inhibitors of the renin-angiotensin system can effectively prevent recurrent stenosis.

Vascular Smooth Muscle Sirtuin-1 Protects Against Aortic Dissection During Angiotensin II–Induced Hypertension

Fry, Jessica L; Shiraishi, Yasunaga; Turcotte, Raphaël; Yu, Xunjie; Gao, Yuan Z; Akiki, Rachid; Bachschmid, Markus; Zhang, Yanhang; Morgan, Kathleen G; Cohen, Richard A; Seta, Francesca
Fonte: John Wiley & Sons, Ltd Publicador: John Wiley & Sons, Ltd
Tipo: Artigo de Revista Científica
EN_US
Relevância na Pesquisa
66.37%
Background: Sirtuin-1 (SirT1), a nicotinamide adenine dinucleotide+–dependent deacetylase, is a key enzyme in the cellular response to metabolic, inflammatory, and oxidative stresses; however, the role of endogenous SirT1 in the vasculature has not been fully elucidated. Our goal was to evaluate the role of vascular smooth muscle SirT1 in the physiological response of the aortic wall to angiotensin II, a potent hypertrophic, oxidant, and inflammatory stimulus. Methods and Results: Mice lacking SirT1 in vascular smooth muscle (ie, smooth muscle SirT1 knockout) had drastically high mortality (70%) caused by aortic dissection after angiotensin II infusion (1 mg/kg per day) but not after an equipotent dose of norepinephrine, despite comparable blood pressure increases. Smooth muscle SirT1 knockout mice did not show any abnormal aortic morphology or blood pressure compared with wild-type littermates. Nonetheless, in response to angiotensin II, aortas from smooth muscle SirT1 knockout mice had severely disorganized elastic lamellae with frequent elastin breaks, increased oxidant production, and aortic stiffness compared with angiotensin II–treated wild-type mice. Matrix metalloproteinase expression and activity were increased in the aortas of angiotensin II–treated smooth muscle SirT1 knockout mice and were prevented in mice overexpressing SirT1 in vascular smooth muscle or with use of the oxidant scavenger tempol. Conclusions: Endogenous SirT1 in aortic smooth muscle is required to maintain the structural integrity of the aortic wall in response to oxidant and inflammatory stimuli...

Larger Anti-adipogenic Effect of Angiotensin II on omental preadipose cells of obese humans

Acuña, María José; Albala Brevis, Cecilia; Cifuentes, Mariana; Rojas, Cecilia V.; Brücher, Rodrigo
Fonte: NORTH AMER ASSOC STUDY OBESITY Publicador: NORTH AMER ASSOC STUDY OBESITY
Tipo: Artículo de revista
EN
Relevância na Pesquisa
66.41%
Objective: The ability to form new adipose cells is important to adipose tissue physiology; however, the mechanisms controlling the recruitment of adipocyte progenitors are poorly understood. A role for locally generated angiotensin II in this process is currently proposed. Given that visceral adipose tissue reportedly expresses higher levels of angiotensinogen compared with other depots and the strong association of augmented visceral fat mass with the adverse consequences of obesity, we studied the role of angiotensin II in regulating adipogenic differentiation in omental fat of obese and non-obese humans. Research Methods and Procedures: The angiotensin II effect on adipose cell formation was evaluated in human omental adipocyte progenitor cells that were stimulated to adipogenic differentiation in vitro. The adipogenic response was measured by the activity of the differentiation marker glycerol-3-phosphate dehydrogenase. Results: Angiotensin II reduced the adipogenic response of adipocyte progenitor cells, and the extent of the decrease correlated directly with the subjects’ BMI (p #1; 0.01, R2 #1; 0.30). A 56.3 #2; 3.4% and 44.5 #2; 2.7% reduction of adipogenesis was found in obese and non obese donors’ cells...

Effects of angiotensin II in the vascular system; Efectos de la angiotensina II en el sistema cardiovascular; EFEITOS DA ANGIOTENSINA II NO SISTEMA CARDIOVASCULAR

Trapp, Sílvia Manduca; Universidade Norte do Paraná, UNOPAR, Paraná, PR; Vailati, Maria do Carmo Fernandez; FMVZ-Unesp, Botucatu; Matsubara, Beatriz Bojikian; Faculdade de Medicina de Botucatu, UNESP, Campus de Botucatu; Schwartz, Denise Saretta; Facul
Fonte: UFPR Publicador: UFPR
Tipo: info:eu-repo/semantics/article; info:eu-repo/semantics/publishedVersion; Artigo Avaliado pelos Pares Formato: application/pdf
Publicado em 16/06/2010 POR
Relevância na Pesquisa
66.44%
Angiotensin is an important peptide of renin-angiotensin-aldosterone system. This peptide has an important function on arterial blood pressure regulation and body fluid homeostasis. However, its action on abnormal conditions causes deleterious effects on the cardiovascular system. Vascular resistance, hypertension, vascular and myocytes hipertrophy, production of free radicals and pro-inflammatory substances are some of the actions of angiotensin II that can result on cardiovascular remodeling. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptors antagonists, antiinflammatories and antioxidants are used clinically and/or experimentally to prevent or reduce the effects of angiotensin II. The purpose of this work is to review the actions and interactions of angiotensin II on the cardiovascular system, as well as the therapeutic measures employed for the control of these effects.; La angiontesina II es el principal péptido del sistema renina-angiotensina-aldosterona. Este péptido tiene un papel importante en la regulación de la presión sanguínea y la homeostasis de los líquidos corporales. Sin embargo, su actuación en condiciones anormales genera efectos en detrimento del sistema cardiovascular. La resistencia vascular...