Publications by authors named "Andreia C Alzamora"

Objective: The aim was to investigate the intergenerational inheritance induced by a high-fat diet on sensitivity to insulin and leptin in the hypothalamic control of satiety in second-generation offspring, which were fed a control diet.

Methods: Progenitor rats were fed a high-fat or a control diet for 59 d until weaning. The first-generation and second-generation offspring were fed the control diet until 90 d of age.

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Psidium guajava (guava) leaves extract displays anti-hypertensive properties by mechanisms not yet fully understood. 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.

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New Findings: What is the central question of this study? How does swimming exercise training impact hydro-electrolytic balance, renal function, sympathetic contribution to resting blood pressure and cerebrospinal fluid (CSF) [Na ] in rats fed a high-sodium diet from weaning? What is the main finding and its importance? An exercise-dependent reduction in blood pressure was associated with decreased CSF [Na ], sympathetically driven vasomotor tonus and renal fibrosis indicating that the anti-hypertensive effects of swimming training in rats fed a high-sodium diet might involve neurogenic mechanisms regulated by sodium levels in the CSF rather than changes in blood volume.

Abstract: 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.

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In previous studies we have shown that oral Ang-(1-7) has a beneficial therapeutic effect on cardiometabolic disturbances present in metabolic syndrome (MetS). Based on the fact that Ang-(1-7) acts through release of nitric oxide (NO), a new peptide, A-1317 was engineered adding the amino acid L-Arginine, the NO precursor, to the N-terminal portion of the Ang-(1-7). Therefore, in a single molecule the substrate and the activator of NO are combined.

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Hypertension is associated with increased central activity of the renin-angiotensin system (RAS) and oxidative stress. Here, we evaluated whether reactive species and neurotransmitters could contribute to the hypotensive effect induced by angiotensin (Ang) II and Ang-(1-7) at the caudal ventrolateral medulla (CVLM) in renovascular hypertensive rats (2K1C). Therefore, we investigated the effect of Ang II, Ang-(1-7), and the Ang-(1-7) antagonist A-779 microinjected before and after CVLM microinjection of the nitric oxide (NO)-synthase inhibitor, (L-NAME), vitamin C (Vit C), bicuculline, or kynurenic acid in 2K1C and SHAM rats.

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Aim: To evaluate physical fitness and cardiovascular effects in rats with renovascular hypertension, two kidneys, one clip (2K1C) submitted to voluntary exercise (ExV).

Main Methods: 24 h after surgery (SHAM and 2K1C) rats were submitted to ExV for one week (adaptation). ExV adherent rats were separated into exercise (2K1C-EX and SHAM-EX) or sedentary (2K1C-SED and SHAM-SED) groups.

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Article Synopsis
  • * Female Fischer rats were given either a high-fat or control diet during mating, gestation, and breastfeeding, and the effects on their offspring were analyzed after they were weaned.
  • * Findings showed that the H diet in mothers led to increased metabolic issues in their offspring, including higher levels of plasma leptin, insulin, and glucose, indicating a risk of metabolic syndrome, even when the offspring were later fed a normal diet.
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Background: Arterial hypertension is a precursor to the development of heart and renal failure, furthermore is associated with elevated oxidative markers. Environmental enrichment of rodents increases performance in memory tasks, also appears to exert an antioxidant effect in the hippocampus of normotensive rats.

Objectives: Evaluate the effect of environmental enrichment on oxidative stress in the ventrolateral medulla, heart, and kidneys of renovascular hypertensive rats.

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In prevention studies of metabolic syndrome (MetS), Ang-(1-7) has shown to improve the insulin signaling. We evaluated the HPCD/Ang-(1-7) treatment on lipid metabolism, renin-angiotensin system (RAS) components, oxidative stress, and insulin pathway in the liver and gastrocnemius muscle and hepatic steatosis in rats with established MetS. After 7 weeks of high-fat (FAT) or control (CT) diets, rats were treated with cyclodextrin (HPCD) or HPCD/Ang-(1-7) in the last 6 weeks.

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Article Synopsis
  • The study investigates the effects of oral Angiotensin (Ang)-(1-7) on metabolic syndrome (MetS) in rats, focusing on factors like blood pressure, insulin resistance, and inflammation in adipose tissue.
  • Rats were divided into control and high-fat diet groups, with one group receiving Ang-(1-7) treatment, and various biochemical and histological assessments were conducted after 13 weeks.
  • Results showed that Ang-(1-7) treatment reduced body fat, inflammation, and improved metabolic markers compared to untreated rats with MetS, suggesting its potential therapeutic benefits for managing obesity-related conditions.
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Physical training (PT) has been considered as a treatment in metabolic syndrome (MS), since it induces thermogenic activity in brown (BAT) and white (WAT) adipose tissues. We evaluated the therapeutic effect of PT on activity of WAT and BAT in rats with MS induced by high-fat diet (30% lard) for 13 weeks and submitted, for the last 6 weeks, to swimming or kept sedentary (SED) rats. MS-SED rats compared to control diet (CT-SED) rats showed low physical fitness and high levels of glucose, insulin, homeostasis evaluation of insulin resistance (HOMA-IR), homeostasis evaluation of the functional capacity of β-cells (HOMA-β), and blood pressure.

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The renin-angiotensin system (RAS) is a key player in the control of the cardiovascular system and hydroelectrolyte balance, with an influence on organs and functions throughout the body. The classical view of this system saw it as a sequence of many enzymatic steps that culminate in the production of a single biologically active metabolite, the octapeptide angiotensin (ANG) II, by the angiotensin converting enzyme (ACE). The past two decades have revealed new functions for some of the intermediate products, beyond their roles as substrates along the classical route.

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Article Synopsis
  • The study examined how a high sodium diet affects hypertension in male Wistar rats from weaning to adulthood, showing significant differences in blood pressure and kidney function compared to a regular sodium diet.
  • Rats on a high sodium diet had increased water intake, urine output, and sodium excretion, resulting in a 13.8% higher blood pressure; ganglionic blockade further lowered their blood pressure significantly.
  • The findings suggest that chronic salt intake leads to hypertension through neurogenic mechanisms, with alterations seen in central nervous system sodium and potassium levels, but no major changes in kidney structure or function.
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Oxidative stress, physical inactivity and high-fat (FAT) diets are associated with hepatic disorders such as metabolic syndrome (MS). The therapeutic effects of physical training (PT) were evaluated in rats with MS induced by FAT diet for 13 weeks, on oxidative stress and insulin signaling in the liver, during the last 6 weeks. FAT-sedentary (SED) rats increased body mass, retroperitoneal fat, mean arterial pressure (MAP) and heart rate (HR), and total cholesterol, serum alanine aminotransferase, glucose and insulin.

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There is evidence that diets rich in salt or simple sugars as fructose are associated with abnormalities in blood pressure regulation. However, the mechanisms underlying pathogenesis of salt- and fructose-induced kidney damage and/or consequent hypertension yet remain largely unexplored. Here, we tested the role of oxidative state as an essential factor along with high salt and fructose treatment in causing hypertension.

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Redox imbalance in regions of the CNS controlling blood pressure is increasingly recognized as a leading factor for hypertension. Nucleus tractus solitarius (NTS) of the dorsomedial medulla is the main region receiving excitatory visceral sensory inputs that modulate autonomic efferent drive to the cardiovascular system. This study sought to determine the capacity of reduced glutathione, a major bioactive antioxidant, to modulate NTS-mediated control of cardiovascular function in unanaesthetized rats.

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What is the central question of this study? In this study, we sought to investigate whether cardiovascular responses to peripheral chemoreflex activation of rats recovered from protein restriction are related to activation of AT receptors. What is the main finding and its importance? This study highlights the fact that angiotensinergic mechanisms activated by AT receptors do not support increased responses to peripheral chemoreflex activation by KCN in rats recovered from protein restriction. Also, we found that protein restriction led to increased resting ventilation in adult rats, even after recovery.

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The central and peripheral renin-angiotensin systems are known for playing a key role in cardiovascular control. In the present study, we evaluated the hemodynamic effects produced by nanoinjections of angiotensin II (Ang II) or angiotensin-(1-7) [Ang-(1-7)] into the rostral ventrolateral medulla (RVLM) of adult male normotensive (Wistar-WT) and spontaneously hypertensive rats (SHR). Animals were anesthetized (urethane 1.

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Background: The metabolic syndrome (MS) is characterized by variable coexistence of metabolic and pathophysiological alterations which are important risk factors for developing of type II diabetes and/or cardiovascular diseases. Increased of MS patients in worldwide has stimulated the development of experimental models. However, it is still challenging to find an dietetic model that most closely approximates human MS and, in addition, is not yet fully established the effect of different diets of MS in lipid metabolism in rats of different ages.

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Aims: The nonpeptide Ang-(1-7) analog, AVE 0991, is recognized as having beneficial cardiovascular effects similar to those induced by Ang-(1-7). In this study, we evaluated the effects of AVE 0991 on cardiovascular functions and on cardiac and renal remodeling in rats with 2K1C renovascular hypertension.

Main Methods: Fisher rats underwent surgery to induce 2K1C renovascular hypertension and were then treated with AVE 0991 (1 or 3mg/kg) for 28days.

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Hypertension 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.

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In 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 AT1 receptor antagonist, Losartan, and Ang-(1-7) Mas antagonist, A-779, respectively.

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We determined the effect of microinjection of ANG-(1-7) and ANG II into two key regions of the medulla that control the circulation [rostral and caudal ventrolateral medulla (RVLM and CVLM, respectively)] on baroreflex control of heart rate (HR) in anesthetized rats. Reflex bradycardia and tachycardia were induced by increases and decreases in mean arterial pressure produced by intravenous phenylephrine and sodium nitroprusside, respectively. The pressor effects of ANG-(1-7) and ANG II (25 pmol) after RVLM microinjection (11 +/- 0.

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