Navegando por Autor "Machado, Raquel do Pilar"
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Item Altered renal response to acute volume expansion in transgenic rats harboring the human tissue kallikrein gene.(2005) Passaglio, Kátia Tomagnini; Baltatu, Ovidiu; Machado, Raquel do Pilar; Reis, Adelina Martha dos; Pesquero, João Bosco; Bader, Michael; Santos, Robson Augusto Souza dosThe renal response to acute volume expansion was investigated in transgenic (TGR) rats harboring the human tissue kallikrein gene. After a primer injection of 0.9% NaCl (3 ml/100 g, i.v), Sprague–Dawley (SD) or TGR rats received a continuous infusion of 0.9% NaCl (15 Al/ 100 g/min, i.a.) through a catheter placed into the carotid artery. Acute volume expansion was produced by a second injection of 0.9% NaCl (2 ml/100 g, i.v.) 65 min after the first injection. Plasma vasopressin (AVP) and atrial natriuretic peptide (ANP) concentration was measured before and within 10 min of volume expansion. TGR animals presented a blunted response to acute volume expansion evidenced by an attenuated increase in total and fractional water and sodium excretion. Before or after volume expansion, plasma AVP and ANP did not differ between SD and TGR. Pre-treatment with the BK-B2 antagonist HOE-140 (7.5 Ag/100 g. i.a) partially improved the renal response of TGRs and severely blunted the response in SD rats. These data show that TGR (hKLK1) rats have an impaired renal response to acute volume expansion that can not be accounted for by changes in the release of AVP or ANP.Item Angiotensin-(1-7) antagonist, A-779, microinjection into the caudal ventrolateral medulla of renovascular hypertensive rats restores baroreflex bradycardia.(2009) Cangussu, Luiza Michelle; Castro, Uberdan Guilherme Mendes de; Machado, Raquel do Pilar; Silva, Marcelo Eustáquio; Ferreira, Patrícia Maria; Santos, Robson Augusto Souza dos; Santos, Maria José Campagnole dos; Alzamora, Andréia CarvalhoIn the present study we evaluated the effect of caudal ventrolateral medulla (CVLM) microinjection of the main angiotensin (Ang) peptides, Ang II and Ang-(1-7), and their selective antagonists on baseline arterial pressure (AP) and on baroreceptor-mediated bradycardia in renovascular hypertensive rats (2K1C). Microinjection of Ang II and Ang-(1-7) into the CVLM of 2K1C rats produced similar decrease in AP as observed in Sham rats. In both Sham and 2K1C, the hypotensive effect of Ang II and Ang-(1-7) at the CVLM was blocked, for up to 30 min, by previous CVLM microinjection of the Ang II AT 1 receptor antagonist, Losartan, and Ang-(1-7) Mas antagonist, A-779, respectively. As expected, the baroreflex bradycardia was lower in 2K1C in comparison to Sham rats. CVLM microinjection of A-779 improved the sensitivity of baroreflex bradycardia in 2K1C hypertensive rats. In contrast, Losartan had no effect on the baroreflex bradycardia in either 2K1C or Sham rats. These results suggest that Ang-(1-7) at the CVLM may contribute to the low sensitivity of the baroreflex control of heart rate in renovascular hypertensive ratsItem Angiotensin-(1-7) is an endogenous ligand for the G protein-coupled receptor Mas.(2003) Santos, Robson Augusto Souza dos; Silva, Ana Cristina Simões e; Maric, Christine; Rabelo, Denise Maria Rover da Silva; Machado, Raquel do Pilar; Buhr, Insa de; Walther, Silvia Heringer; Pinheiro, Sérgio Veloso Brant; Lopes, Miriam Teresa Paz; Bader, Michael; Mendes, Elizabeth Pereira; Lemos, Virgina Soares; Santos, Maria José Campagnole dos; Schultheiss, Heinz-Peter; Speth, Robert; Walther, ThomasThe renin–angiotensin system plays a critical role in blood pressure control and body fluid and electrolyte homeostasis. Besides angiotensin (Ang) II, other Ang peptides, such as Ang III [Ang-(2–8)], Ang IV [Ang-(3–8)], and Ang-(1–7) may also have important biological activities. Ang-(1–7) has become an angiotensin of interest in the past few years, because its cardiovascular and baroreflex actions counteract those of Ang II. Unique angiotensin-binding sites specific for this heptapeptide and studies with a selective Ang-(1–7) antagonist indicated the existence of a distinct Ang-(1–7) receptor. We demonstrate that genetic deletion of the G proteincoupled receptor encoded by the Mas protooncogene abolishes the binding of Ang-(1–7) to mouse kidneys. Accordingly, Mas-deficient mice completely lack the antidiuretic action of Ang-(1–7) after an acute water load. Ang-(1–7) binds to Mas-transfected cells and elicits arachidonic acid release. Furthermore, Mas-deficient aortas lose their Ang-(1–7)-induced relaxation response. Collectively, these findings identify Mas as a functional receptor for Ang-(1–7) and provide a clear molecular basis for the physiological actions of this biologically active peptide.Item Avaliação da sensibilidade do barorreflexo em modelo experimental de hipercolesterolemia co-existente com hipertensão renal.(Programa de Pós-Graduação em Ciências Biológicas. Núcleo de Pesquisas em Ciências Biológicas, Pró-Reitoria de Pesquisa e Pós Graduação, Universidade Federal de Ouro Preto., 2006) Spinassé, Giselle Menelli; Machado, Raquel do PilarHipercolesterolemia (HC) e hipertensão arterial (HA) são os principais fatores de risco para o desenvolvimento e progressão da doença cardíaca aterosclerótica, e sua co-existência foi associada a uma alta incidência de eventos cardíacos em estudos clínicos. A sensibilidade do barorreflexo tem importante valor prognóstico para diversas condições patofisiológicas cardiovasculares. Assim, este trabalho teve como objetivo avaliar a sensibilidade do barorreflexo em ratos apresentando simultaneamente HC e HA. Foram utilizados ratos Wistar e Fisher. Os animais foram submetidos à dieta hipercolesterolêmica (Hiper) (1% de colesterol, 25% de óleo de soja) ou controle (Cont) 30 dias antes e 30 dias após cirurgia 2R1C (2 rins, 1 clip) para produção da hipertensão renal ou cirurgia fictícia (Sham). Com o objetivo de obter níveis maiores de colesterol sérico, ratos sham (Fisher) foram submetidos à dieta Hiper com adição de 0,3% de deoxicolato de sódio (DS). A sensibilidade do barorreflexo foi determinada através de alterações de pressão arterial (PA) induzidas por injeções endovenosas, em bolus, de doses crescentes de fenilefrina e nitroprussiato de sódio, para avaliação dos componentes bradicárdicos e taquicárdicos, respectivamente. A dieta Hiper não elevou os níveis séricos de colesterol nos ratos Wistar (45,9±18,5 mg/dL, ShamHiper e 74,6±mg/dL, 2R1CHiper) em relação ao controle (54,4±21,6 mg/dL, ShamCont e 50,6±17 mg/dL, 2R1CCont). No entanto, os ratos Fisher desenvolveram HC (98,06±28,59 mg/dL, ShamHiper e 100,11±25,47 mg/dL, 2R1CHiper) em relação ao controle (75,2±23,1 mg/dL, ShamCont e 62,7±12,7 mg/dL, 2R1CCont), além de desenvolverem HA (142,2±9,7 mmHg, 2R1CCont e 143,8±12 mmHg, 2R1CHiper) comparados aos animais sham (101,4±10,5 mmHg, ShamCont e 99,5±11,1 mmHg, ShamHiper), adequando-se ao modelo proposto. A dieta Hiper com DS não elevou significativamente os níveis séricos de colesterol dos ratos sham Fisher (99,3±8,2 mg/dL) em relação à dieta Hiper sem DS (98,1±10,8 mg/dL). Os ratos Fisher 2R1C apresentaram freqüência cardíaca (FC) elevada (449,4±39 bpm, 2R1CCont e 464,0±29,8 bpm, 2R1CHiper) em relação aos animais sham (401,7±35,8 bpm, ShamCont e 378,1±32,6 bpm, ShamHiper). Nos ratos Fisher a sensibilidade bradicárdica foi reduzida em animais submetidos à hipertensão renovascular (HR), associada ou não à HC, enquanto a sensibilidade taquicárdica não foi alterada significativamente em nenhum grupo avaliado. Nossos dados sugerem que, no modelo proposto, o aumento da FC associado à diminuição da sensibilidade bradicárdica e à manutenção da sensibilidade taquicárdica podem estar correlacionados a aumentos da atividade simpática e principalmente à redução da atividade parassimpática, uma vez que a alteração é mais evidente frente a aumentos do que a quedas da PA. Sugerem também que a HC não afeta a sensibilidade barorreflexa, reduzida em decorrência da HR, no organismo onde HC e HR co-existem.Item Cardiac and renal effects induced by different exercise workloads in renovascular hypertensive rats.(2011) Soares, Everton Rocha; Lima, Wanderson Geraldo de; Machado, Raquel do Pilar; Carneiro, Cláudia Martins; Silva, Marcelo Eustáquio; Rodrigues, Míriam Carmo; Castro, Uberdan Guilherme Mendes de; Santos, Robson Augusto Souza dos; Santos, Maria José Campagnole dos; Alzamora, Andréia CarvalhoWe examined the effect of exercise training (Ex) without (Ex 0%) or with a 3% workload (Ex 3%) on different cardiac and renal parameters in renovascular hypertensive (2K1C) male Fisher rats weighing 150-200 g. Ex was performed for 5 weeks, 1 h/day, 5 days/week. Ex 0% or Ex 3% induced similar attenuation of baseline mean arterial pressure (MAP, 119 ± 5 mmHg in 2K1C Ex 0%, N = 6, and 118 ± 5 mmHg in 2K1C Ex 3%, N = 11, vs 99 ± 4 mmHg in sham sedentary (Sham Sed) controls, N = 10) and heart rate (HR, bpm) (383 ± 13 in 2K1C Ex 0%, N = 6, and 390 ± 14 in 2K1C Ex 3%, N = 11 vs 371 ± 11 in Sham Sed, N = 10). Ex 0%, but not Ex 3%, improved baroreflex bradycardia (0.26 ± 0.06 ms/mmHg, N = 6, vs 0.09 ± 0.03 ms/mmHg in 2K1C Sed, N = 11). Morphometric evaluation suggested concentric left ventricle hypertrophy in sedentary 2K1C rats. Ex 0% prevented concentric cardiac hypertrophy, increased cardiomyocyte diameter and decreased cardiac vasculature thickness in 2K1C rats. In contrast, in 2K1C, Ex 3% reduced the concentric remodeling and prevented the increase in cardiac vasculature wall thickness, decreased the cardiomyocyte diameter and increased collagen deposition. Renal morphometric analysis showed that Ex 3% induced an increase in vasculature wall thickness and collagen deposition in the left kidney of 2K1C rats. These data suggest that Ex 0% has more beneficial effects than Ex 3% in renovascular hypertensive rats.Item Evidence for a role of AT 2 receptors at the CVLM in the cardiovascular changes induced by low-intensity physical activity in renovascular hypertensive rats.(2007) Rodrigues, Míriam Carmo; Santos, Maria José Campagnole dos; Machado, Raquel do Pilar; Silva, Marcelo Eustáquio; Rocha, José Luiz Marques; Ferreira, Patrícia Maria; Santos, Robson Augusto Souza dos; Alzamora, Andréia CarvalhoIn the present study, we evaluated the involvement of the rennin–angiotensin system (RAS) in the control of the blood pressure (BP), baroreceptor-mediated bradycardia and the reactivity of caudal ventrolateral medulla (CVLM) neurons to Ang II and to AT2 receptor antagonist in sedentary or trained renovascularhypertensive rats. Physical activity did not significantly change the baseline mean arterial pressure (MAP), heart rate (HR) or the sensitivity of the baroreflex bradycardia in normotensive Sham rats. However, in 2K1C hypertensive rats, physical activity induced a significant fall in baseline MAP and HR and produced an improvement of the baroreflex function (bradycardic component). The microinjections of Ang II into the CVLM produced similar decreases in MAP in all groups, Sham and 2K1C, sedentary and trained rats. The hypotensive effect of Ang II at the CVLM was blocked by previous microinjection of the AT2 receptors antagonist, PD123319, in all groups of rats. Unexpectedly, microinjection of PD123319 at the CVLM produced a depres-sor effect in 2K1C sedentary that was attenuated in 2K1C trained rats. No significant changes in MAP were observed after PD123319 i n Sham rats, sedentary or trained. These data showed that low-intensity physical activity is effective in lowering blood pressure and restoring the sensitivity of t he baroreflex bradycardia, however these cardiovascular effects are not accompanied by changes i n the responsiveness to Ang II at CVLM in normotensive or hypertensive, 2K1C rats. In ad dition, the blood pressure changes observed after AT 2 blockade in 2K1C rats suggest that hypertension may trigger an imbalance of AT1 /AT 2 receptors at the CVLM that may be restored, at least in part, by low-intensity physical activityItem Nitric oxide at the CVLM is involved in the attenuation of the reflex bradycardia in renovascular hypertensive rats.(2012) Castro, Uberdan Guilherme Mendes de; Souza, Graziele Galdino de; Machado, Raquel do Pilar; Isoldi, Mauro César; Silva, Marcelo Eustáquio; Nadu, Ana Paula; Souza, Luiz Eduardo de; Santos, Robson Augusto Souza dos; Santos, Maria José Campagnole dos; Alzamora, Andréia CarvalhoHypertension is associated to an increase in central oxidative stress and an attenuation of the baroreflex control of arterial pressure. The present study evaluated the effect of alterations in the levels of nitric oxide (NO) and superoxide anion in the caudal ventrolateral medulla (CVLM), a key area of the brainstem for the baroreflex control of arterial pressure, in renovascular hypertensive rats (2K1C). Baseline mean arterial pressure (MAP), heart rate (HR), and reflex bradycardia were evaluated 30 days after renal artery occlusion in anesthetized (urethane, 1.2 g/kg, i.p.) 2K1C or normotensive (SHAM) rats. The MAP, HR, and baroreflex control of HR were evaluated before and after CVLM microinjections of the non-selective NOS inhibitor L-NAME (10 nmol), the NO precursor L-ARG (50 nmol), or the antioxidant ascorbic acid, Vit C (10 nmol). In both 2K1C and SHAM animals, CVLM microinjection of L-NAME produced a decrease in MAP, whereas L-ARG induced a significant increase in MAP. However, microinjection of Vit C into the CVLM produced a decrease in MAP and HR only in 2K1C and not in SHAM rats. Cardiovascular effects produced by microinjection of L-ARG into the CVLM were abolished by prior microinjection of L-NAME in the CVLM of 2K1C and SHAM rats. Microinjection of L-NAME into the CVLM increased the sensitivity of reflex bradycardia in 2K1C animals. In contrast, the CVLM microinjection of L-ARG reduced reflex bradycardia only in SHAM rats. Vit C in the CVLM did not change reflex bradycardia in either 2K1C or in SHAM rats. These results suggest that increased oxidative stress in the CVLM during hypertension contributes to the reduced baroreflex sensitivity and to maintain hypertension in the 2K1C model.Item Quantitative analysis of cardiac lesions in chronic canine chagasic cardiomyopathy.(2002) Caliari, Marcelo Vidigal; Machado, Raquel do Pilar; Lana, Marta de; Cajá, Rosângela Aparecida França; Carneiro, Cláudia Martins; Bahia, Maria Terezinha; Santos, César Augusto Bueno dos; Magalhães, Gustavo Albergaria; Sampaio, Ivan Barbosa Machado; Tafuri, Washington LuizLesions observed in chronic chagasic cardiopathy frequently produce electrocardiographic alterations and affect cardiac function. Through a computerized morphometrical analysis we quantified the areas occupied by cardiac muscle, connective and adipose tissues in the right atrium of dogs experimentally infected with Trypanosoma cruzi. All of the infected dogs showed chronic myocarditis with variable reduction levels of cardiac muscle, fibrosis and adipose tissue replacement. In the atrial myocardium of dogs infected with Be78 and Be62 cardiac muscle represented 34 and 50%, fibrosis 28 and 32% and adipose tissue 38 and 18%, respectively. The fibrosis observed was both diffuse and focal and mostly intrafascicular, either partially or completely interrupting the path of muscle bundles. Such histological alterations probably contributed to the appearance of electrocardiographic disturbances verified in 10 out 11 dogs which are also common in human chronic chagasic cardiopathy. Fibrosis was the most important microscopic occurrence found since it produces rearrangements of collagen fibers in relation to myocardiocytes which causes changes in anatomical physiognomy and mechanical behavior of the myocardium. These abnormalities can contribute to the appearance of cardiac malfunction, arrhythmias and congestive cardiac insufficiency as observed in two of the analyzed dogs. Strain Be78 caused destruction of atrial cardiac muscle higher than that induced by strain Be62.Item Renovascular hypertension increases serum TNF and CX3CL1 in experimental Trypanosoma cruzi infection.(2018) Silva, M. C.; Azevedo, Maíra Araújo; Figueiredo, Vivian Paulino; Moura Junior, Manoel Ramos de; Coelho Junior, Diógenes; Martinelli, Patrícia Massara; Machado, Raquel do Pilar; Alzamora, Andréia Carvalho; Silva, André Talvani Pedrosa daTrypanosoma cruzi triggers a progressive inflammatory response affecting cardiovascular functions in humans and experimental models. Angiotensin II, a key effector of the renin-angiotensin system, plays roles in mediating hypertension, heart failure, and inflammatory responses. T. cruzi and AngII can induce inflammatory responses by releasing inflammatory mediators. The aim of this study was to evaluate systemic AngII, tumor necrosis factor (TNF), and CX3CL1 mediators in a two-kidney one-clip (2K1C) renovascular hypertension model using Wistar rats infected with T. cruzi. Our data showed an increase in serum AngII in uninfected and T. cruzi-infected rats 1 week after 2K1C surgery compared to non-2K1C (Sham) animals. The baseline systolic blood pressure was higher in both uninfected and infected 2K1C rats. Despite no difference in circulating parasites in the acute phase of infection, elevated serum TNF and CX3CL1 were observed at 8 weeks post-infection in 2K1C rats in association with higher cardiac inflammatory infiltration. In summary, AngII-induced hypertension associated with T. cruzi infection may act synergistically to increase TNF and CX3CL1 in the 2K1C rat model, thereby intensifying cardiac inflammatory infiltration and worsening the underlying inflammation triggered by this protozoan.