Browsing by Author "Antunes, Vagner Roberto"

Now showing 1 - 4 of 4
  • No Thumbnail Available
    Item
    Effects of Psidium guajava L. leaves extract on blood pressure control and IL-10 production in salt-dependent hypertensive rats.
    (2022) Braga, Daiane Cristina de Assis; Gomes, Paula Magalhães; Batista, Marcos Adriano Carlos; Souza, Jaqueline Aparecida de; Bastos, Juliana Cristina Santos Almeida; Dôres, Rosana Gonçalves Rodrigues das; Alzamora, Andréia Carvalho; Souza, Gustavo Henrique Bianco de; Moura, Sandra Aparecida Lima de; Silva, André Talvani Pedrosa da; Antunes, Vagner Roberto; Cardoso, Leonardo Máximo
    Psidium guajava (guava) leaves extract displays anti-hypertensive properties by mechanisms not yet fully un- derstood. Here, we investigated whether sympathetic drive and immune signaling mechanisms are involved with the antihypertensive effect of the guava extract in a model of salt-dependent hypertension. Raw guava extract (rPsE) was characterized by colorimetric and UPLC-MS techniques. Two doses of rPsE (100 and 200 mg/kg) were evaluated for anti-hypertensive effect using a suspension system (PsE). Weaned male Wistar rats were put on a high-salt diet (HSD, 0.90 % Na+) for 16 weeks and received gavages of PsE for the last 4 weeks. Blood pressure (BP) was measured at the end of treatment in conscious rats. The neurogenic pressor effect was assessed by ganglionic blockade with hexamethonium. Autonomic modulation of heart rate was evaluated by spectral analysis. The effects of orally administered PsE on lumbar sympathetic nerve activity (LSNA) were assessed in anesthetized rats. Blood IL-10, IL-17A, and TNF were measured. The increased neurogenic pressor effect of HSD rats was reduced by PsE 100 mg/kg, but not by 200 mg/kg. PsE (200 mg/kg) administration in anesthetized rats produced a greater fall in BP of HSD rats compared to standard salt diet (SSD) rats. PsE hypotensive response elicited an unproportionable increase in LSNA of HSD rats compared to SSD rats. PsE (200 mg/kg) increased plasma concentrations of IL-10 but had no effect on TNF or IL-17A. Our data indicate that the antihypertensive effects of PsE may involve autonomic mechanisms and immunomodulation by overexpression of IL-10 in salt- dependent hypertensive rats.
  • No Thumbnail Available
    Item
    Quimiorreflexo e receptores AT1 : papel no controle cardiovascular de animais recuperados da restrição proteica sedentários e treinados.
    (2015) Sá, Renato Willian Martins; Cardoso, Leonardo Máximo; Oliveira, Lenice Kappes Becker; Antunes, Vagner Roberto
    Neste trabalho investigamos o quimiorreflexo arterial e o possível envolvimento de receptores AT1 na sua modulação em ratos recuperados da restrição proteica pós desmame submetidos ao treinamento físico crônico. Para tanto, ratos Fischer foram divididos em grupos controles sedentários (C105 S) e treinados (C105 T), e recuperados sedentários (R-RP S) e treinados (R-RP T). Os ratos recuperados foram alimentados com dieta hipoproteica (caseína - 8%) por 35 dias após o desmame e, em seguida, recuperados com dieta normoproteica (20%) por 70 dias. Os grupos controles receberam apenas dieta normoproteica por 105 dias. O programa de treinamento físico de natação foi realizado diariamente (5 dias por semana) durante oito semanas, cumprindo normativas de intensidade e volume progressivos. 48 horas após a cirurgia de canulação, a pressão arterial média (PAM) e a frequência cardíaca (FC) foram registradas em ratos acordados. O quimiorreflexo foi estimulado por injeções intravenosas (i.v.) de KCN (20-160μg/kg) imediatamente antes (basal) e após 75 minutos do bloqueio de receptores AT1 com losartan (20 mg/kg, i.v.). Em ratos sedentários, as respostas pressora e bradiarrítmica evocadas pela dose de 60 μg/kg de KCN foram maiores no grupo R-RP S em relação ao grupo C105 S [25 ± 5 mmHg; -27 ± 9 bpm (C105 S) e 45 ± 4 mmHg e -76 ± 14 bpm (R-RP S)]. A administração de losartan não modificou estas respostas. Em ratos treinados, não foram observadas diferenças na resposta pressora para a mesma dose de KCN entre os grupos R-RP T e C105 T. Contudo, a resposta bradiarrítmica foi maior no grupo C105 T em relação ao grupo R-RP T [-166 ± 44 bpm (C105 T) e -44 ± 36 bpm (R-RP T). O losartan também não alterou a magnitude destas respostas. Em conclusão, a restrição proteica seguida pela recuperação alimentar eleva a sensibilidade do componente cardiovascular do quimiorreflexo arterial por mecanismos que parecem não depender de receptores AT1. O treinamento físico crônico foi capaz de normalizar a sensibilidade do componente pressor do quimiorreflexo arterial em ratos recuperados de restrição proteica pós-desmame sugerindo que o treinamento físico possa estar corrigindo ou compensando alterações do quimiorreflexo arterial geradas pela restrição/recuperação.
  • No Thumbnail Available
    Item
    Swimming training improves cardiovascular autonomic dysfunctions and prevents renal damage in rats fed a high-sodium diet from weaning.
    (2020) Souza, Jaqueline Aparecida de; Oliveira, Lenice Kappes Becker; Batista, Marcos Adriano Carlos; Braga, Daiane Cristina de Assis; Gomes, Paula Magalhães; Alzamora, Andréia Carvalho; Vieira, Maria Aparecida Ribeiro; Lima, Wanderson Geraldo de; Andrade, Marina Gonçalves Caetano; Sanches, Bruno de Lima; Totou, Nádia Lúcia; Martins Junior, Francisco de Assis Dias; Oliveira, Lisandra Brandino de; Antunes, Vagner Roberto; Cardoso, Leonardo Máximo
    High sodium intake is an important factor associated with hypertension. High-sodium intake with exercise training can modify homeostatic hydro-electrolytic balance, but the effects of this association are mostly unknown. In this study, we sought to investigate the effects of swimming training (ST) on cerebrospinal fluid (CSF) Na+ concentration, sympathetic drive, blood pressure (BP) and renal function of rats fed a 0.9% Na+ (equivalent to 2% NaCl) diet with free access to water for 22 weeks after weaning. Male Wistar rats were assigned to two cohorts: (1) fed standard diet (SD) and (2) fed high-sodium (HS) diet. Each cohort was further divided into trained and sedentary groups. ST normalised BP levels of HS rats as well as the higher sympathetically related pressor activity assessed by pharmacological blockade of ganglionic transmission (hexamethonium). ST preserved the renal function and attenuated the glomerular shrinkage elicited by HS. No change in blood volume was found among the groups. CSF [Na+] levels were higher in sedentary HS rats but were reduced by ST. Our findings showed that ST effectively normalised BP of HS rats, independent of its effects on hydro-electrolytic balance, which might involve neurogenic mechanisms regulated by Na+ levels in the CSF as well as renal protection.
  • No Thumbnail Available
    Item
    The gut-brain axis and sodium appetite : can inflammation-related signaling influence the control of sodium intake?
    (2022) Freitas, Flávio Eduardo Dias Araújo; Batista, Marcos Adriano Carlos; Braga, Daiane Cristina de Assis; Oliveira, Lisandra Brandino de; Antunes, Vagner Roberto; Cardoso, Leonardo Máximo
    Sodium is the main cation present in the extracellular fluid. Sodium and water content in the body are responsible for volume and osmotic homeostasis through mechanisms involving sodium and water excretion and intake. When body sodium content decreases below the homeostatic threshold, a condition termed sodium deficiency, highly motivated sodium seeking, and intake occurs. This is termed sodium appetite. Classically, sodium and water intakes are controlled by a number of neuroendocrine mechanisms that include signaling molecules from the renin-angiotensin-aldosterone system acting in the central nervous system (CNS). However, recent findings have shown that sodium and water intakes can also be influenced by inflammatory agents and mediators acting in the CNS. For instance, central infusion of IL-1β or TNF-α can directly affect sodium and water consumption in animal models. Some dietary conditions, such as high salt intake, have been shown to change the intestinal microbiome composition, stimulating the immune branch of the gut-brain axis through the production of inflammatory cytokines, such as IL-17, which can stimulate the brain immune system. In this review, we address the latest findings supporting the hypothesis that immune signaling in the brain could produce a reduction in thirst and sodium appetite and, therefore, contribute to sodium intake control.