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1.
Cell Biol Int ; 43(8): 890-898, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31062893

RESUMO

The present study aimed to test the hypothesis that increased sodium concentration affects the migratory phenotype of vascular smooth muscle cells (VSMCs) independently of the haemodynamic factors. Cell migration was evaluated by wound-healing assay under the following conditions: high sodium (HS, 160 mM) and control (CT, 140 mM). Cell viability was assessed by annexin V and propidium iodide labeling. Cyclooxygenase-2 (COX-2) gene expression was analysed by reverse transcription polymerase chain reaction. ERK1/2 phosphorylation was assessed by western blot. Exposure of VSMCs to HS reduced migration, and AT1R blockade prevented this response. HS increased COX-2 gene expression, and COX-2 blockade prevented the reduction in VSMC migration induced by HS. HS also increased ERK1/2 phosphorylation, and ERK1/2 inhibition recovered VSMC migration as well as blocked COX-2 gene expression. The TXA2 receptor blocker, but not the prostacyclin receptor blocker, prevented the HS-induced VSMCs migration decrease. HS reduces the migration of VSMCs by increasing COX-2 gene expression via AT1R-ERK1/2 phosphorylation. In addition, increased COX-2 by HS seems to modulate the reduction of VSMCs migration by the TXA2 receptor.


Assuntos
Movimento Celular/efeitos dos fármacos , Músculo Liso Vascular , Miócitos de Músculo Liso/metabolismo , Receptor Tipo 1 de Angiotensina/metabolismo , Sódio/farmacologia , Animais , Células Cultivadas , Ciclo-Oxigenase 2/metabolismo , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Músculo Liso Vascular/citologia , Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso/citologia , Receptores de Tromboxano A2 e Prostaglandina H2/metabolismo , Sódio/química
2.
Clin Physiol Funct Imaging ; 38(3): 468-476, 2018 May.
Artigo em Inglês | MEDLINE | ID: mdl-28444936

RESUMO

The aim of this study was to evaluate the acute effects of high-intensity eccentric exercise (HI-ECC) combined with blood flow restriction (BFR) on muscle damage markers, and perceptual and cardiovascular responses. Nine healthy men (26 ± 1 years, BMI 24 ± 1 kg m- ²) underwent unilateral elbow extension in two conditions: without (HI-ECC) and with BFR (HI-ECC+BFR). The HI-ECC protocol corresponded to three sets of 10 repetitions with 130% of maximal strength (1RM). The ratings of perceived exertion (RPE) and pain (RPP) were measured after each set. Muscle damage was evaluated by range of motion (ROM), upper arm circumference (CIR) and muscle soreness using a visual analogue scale at different moments (pre-exercise, immediately after, 24 and 48 h postexercise). Systolic (SBP), diastolic (DBP), mean blood pressure (MBP) and heart rate (HR) were measured before exercise and after each set. RPP was higher in HI-ECC+BFR than in HI-ECC after each set. Range of motion decreased postexercise in both conditions; however, in HI-ECC+BFR group, it returned to pre-exercise condition earlier (post-24 h) than HI-ECC (post-48 h). CIR increased only in HI-ECC, while no difference was observed in HI-ECC+BFR condition. Regarding cardiovascular responses, MBP and SBP did not change at any moment. HR showed similar increases in both conditions during exercise while DBP decreased only in HI-ECC condition. Thus, BFR attenuated HI-ECC-induced muscle damage and there was no increase in cardiovascular responses.


Assuntos
Hemodinâmica , Contração Muscular , Músculo Esquelético/irrigação sanguínea , Mialgia/prevenção & controle , Percepção da Dor , Treinamento de Resistência/métodos , Torniquetes , Adulto , Pressão Sanguínea , Estudos Cross-Over , Cotovelo , Frequência Cardíaca , Humanos , Masculino , Mialgia/etiologia , Mialgia/fisiopatologia , Resistência Física , Amplitude de Movimento Articular , Fluxo Sanguíneo Regional , Treinamento de Resistência/efeitos adversos , Fatores de Tempo
3.
Int J Sports Physiol Perform ; 13(7): 953-956, 2018 Aug 01.
Artigo em Inglês | MEDLINE | ID: mdl-29182414

RESUMO

PURPOSE: To evaluate whether cell-free DNA (cfDNA) levels increase immediately after an acute light and heavy resistance exercise (RE) bout and whether cfDNA levels are associated with functional muscle capacity up to 48 h after an exercise session. METHODS: Twenty healthy volunteers performed 3 sets of leg-press RE with 80% of 1-repetition maximum (1RM) (RE80) or 40% of 1RM (RE40) with similar exercise volume. Blood lactate was measured after completion of the 3 sets. Creatine kinase, cfDNA, and jump performance were evaluated before (pre) exercise, immediately postexercise (post-0h), and every 24 h until 48 h. RESULTS: Lactate concentration increased similarly in both groups (RE40 4.0 [1.3] mmol/L; RE80 4.8 [1.3] mmol/L). No changes were observed in squat-jump and countermovement-jump performance after RE40; however, both jumps remained reduced until 48 h in the RE80 group. Creatine kinase concentration increased post-24h only in the RE80 group (pre 128.8 [73.7] U/L to post-24h 313.8 [116.4] U/L). cfDNA concentration increased post-0h only in the RE80 group (pre 249.8 [82.3] ng/mL to post-0h 406.3 [67.2] ng/mL). There was a negative correlation between post-0h cfDNA concentration and post-24h squat jump (r = -.521; P = .01) and post-0h cfDNA concentration and post-24h countermovement jump (r = -.539; P = .01). CONCLUSION: cfDNA increases in response to RE intensity even when not performed until exhaustion. cfDNA measured immediately after RE is a promising biomarker for muscle-performance decrement up to 48 h after a RE bout.


Assuntos
Desempenho Atlético/fisiologia , Ácidos Nucleicos Livres/sangue , Músculo Esquelético/lesões , Treinamento de Resistência/efeitos adversos , Adulto , Biomarcadores/sangue , Creatina Quinase/sangue , Humanos , Ácido Láctico/sangue , Masculino , Músculo Esquelético/enzimologia , Músculo Esquelético/fisiologia , Treinamento de Resistência/métodos , Fatores de Tempo , Adulto Jovem
4.
Stem Cells Int ; 2016: 9762959, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-26904133

RESUMO

The endothelial lining of the vasculature is exposed to a large variety of biochemical and hemodynamic stimuli with different gradients throughout the vascular network. Adequate adaptation requires endothelial cells to be highly plastic, which is reflected by the remarkable heterogeneity of endothelial cells in tissues and organs. Hemodynamic forces such as fluid shear stress and cyclic strain are strong modulators of the endothelial phenotype and function. Although endothelial plasticity is essential during development and adult physiology, proatherogenic stimuli can induce adverse plasticity which contributes to disease. Endothelial-to-mesenchymal transition (EndMT), the hallmark of endothelial plasticity, was long thought to be restricted to embryonic development but has emerged as a pathologic process in a plethora of diseases. In this perspective we argue how shear stress and cyclic strain can modulate EndMT and discuss how this is reflected in atherosclerosis and pulmonary arterial hypertension.

5.
Am J Physiol Cell Physiol ; 309(8): C541-50, 2015 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-26246427

RESUMO

Physiological concentrations of angiotensin II (ANG II) upregulate the activity of Na(+)/H(+) exchanger isoform 3 (NHE3) in the renal proximal tubule through activation of the ANG II type I (AT1) receptor/G protein-coupled signaling. This effect is key for maintenance of extracellular fluid volume homeostasis and blood pressure. Recent findings have shown that selective activation of the beta-arrestin-biased AT1 receptor signaling pathway induces diuresis and natriuresis independent of G protein-mediated signaling. This study tested the hypothesis that activation of this AT1 receptor/beta-arrestin signaling inhibits NHE3 activity in proximal tubule. To this end, we determined the effects of the compound TRV120023, which binds to the AT1R, blocks G-protein coupling, and stimulates beta-arrestin signaling on NHE3 function in vivo and in vitro. NHE3 activity was measured in both native proximal tubules, by stationary microperfusion, and in opossum proximal tubule (OKP) cells, by Na(+)-dependent intracellular pH recovery. We found that 10(-7) M TRV120023 remarkably inhibited proximal tubule NHE3 activity both in vivo and in vitro. Additionally, stimulation of NHE3 by ANG II was completely suppressed by TRV120023 both in vivo as well as in vitro. Inhibition of NHE3 activity by TRV120023 was associated with a decrease in NHE3 surface expression in OKP cells and with a redistribution from the body to the base of the microvilli in the rat proximal tubule. These findings indicate that biased signaling of the beta-arrestin pathway through the AT1 receptor inhibits NHE3 activity in the proximal tubule at least in part due to changes in NHE3 subcellular localization.


Assuntos
Arrestinas/metabolismo , Túbulos Renais Proximais/citologia , Receptor Tipo 1 de Angiotensina/fisiologia , Trocadores de Sódio-Hidrogênio/metabolismo , Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia , Animais , Humanos , Concentração de Íons de Hidrogênio , Túbulos Renais Proximais/fisiologia , Masculino , Oligopeptídeos/farmacologia , Ratos , Ratos Sprague-Dawley , Transdução de Sinais , Sódio/metabolismo , Trocador 3 de Sódio-Hidrogênio , Trocadores de Sódio-Hidrogênio/genética , beta-Arrestinas
6.
Am J Physiol Heart Circ Physiol ; 309(4): H543-52, 2015 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-26071549

RESUMO

Left ventricular (LV) hypertrophy is an important physiological compensatory mechanism in response to chronic increase in hemodynamic overload. There are two different forms of LV hypertrophy, one physiological and another pathological. Aerobic exercise induces beneficial physiological LV remodeling. The molecular/cellular mechanisms for this effect are not totally known, and here we review various mechanisms including the role of microRNA (miRNA). Studies in the heart, have identified antihypertrophic miRNA-1, -133, -26, -9, -98, -29, -378, and -145 and prohypertrophic miRNA-143, -103, -130a, -146a, -21, -210, -221, -222, -27a/b, -199a/b, -208, -195, -499, -34a/b/c, -497, -23a, and -15a/b. Four miRNAs are recognized as cardiac-specific: miRNA-1, -133a/b, -208a/b, and -499 and called myomiRs. In our studies we have shown that miRNAs respond to swimming aerobic exercise by 1) decreasing cardiac fibrosis through miRNA-29 increasing and inhibiting collagen, 2) increasing angiogenesis through miRNA-126 by inhibiting negative regulators of the VEGF pathway, and 3) modulating the renin-angiotensin system through the miRNAs-27a/b and -143. Exercise training also increases cardiomyocyte growth and survival by swimming-regulated miRNA-1, -21, -27a/b, -29a/c, -30e, -99b, -100, -124, -126, -133a/b, -143, -144, -145, -208a, and -222 and running-regulated miRNA-1, -26, -27a, -133, -143, -150, and -222, which influence genes associated with the heart remodeling and angiogenesis. We conclude that there is a potential role of these miRNAs in promoting cardioprotective effects on physiological growth.


Assuntos
Cardiomegalia Induzida por Exercícios , Exercício , Hipertrofia Ventricular Esquerda/metabolismo , MicroRNAs/metabolismo , Miócitos Cardíacos/metabolismo , Remodelação Ventricular , Animais , Humanos , MicroRNAs/genética , Miócitos Cardíacos/fisiologia
7.
Int J Mol Sci ; 16(2): 4226-49, 2015 Feb 16.
Artigo em Inglês | MEDLINE | ID: mdl-25690036

RESUMO

Dipeptidyl peptidase IV (DPPIV) is a widely expressed multifunctional serine peptidase that exists as a membrane-anchored cell surface protein or in a soluble form in the plasma and other body fluids. Numerous substrates are cleaved at the penultimate amino acid by DPPIV, including glucagon-like peptide-1 (GLP-1), brain natriuretic peptide (BNP) and stromal cell-derived factor-1 (SDF-α), all of which play important roles in the cardiovascular system. In this regard, recent reports have documented that circulating DPPIV activity correlates with poorer cardiovascular outcomes in human and experimental heart failure (HF). Moreover, emerging evidence indicates that DPPIV inhibitors exert cardioprotective and renoprotective actions in a variety of experimental models of cardiac dysfunction. On the other hand, conflicting results have been found when translating these promising findings from preclinical animal models to clinical therapy. In this review, we discuss how DPPIV might be involved in the cardio-renal axis in HF. In addition, the potential role for DPPIV inhibitors in ameliorating heart disease is revised, focusing on the effects of the main DPPIV substrates on cardiac remodeling and renal handling of salt and water.


Assuntos
Dipeptidil Peptidase 4/metabolismo , Insuficiência Cardíaca/fisiopatologia , Animais , Quimiocina CXCL12/metabolismo , Dipeptidil Peptidase 4/química , Inibidores da Dipeptidil Peptidase IV/uso terapêutico , Peptídeo 1 Semelhante ao Glucagon/uso terapêutico , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/metabolismo , Humanos , Peptídeo Natriurético Encefálico/metabolismo
8.
Cell Physiol Biochem ; 33(3): 657-69, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-24642957

RESUMO

BACKGROUND: Myocardial infarction (MI) is accompanied by cardiac growth, increased collagen deposition, cell death and new vascularization of the cardiac tissue, which results in reduced ventricular compliance. The MiRNA-29 family (29a, 29b, and 29c) targets mRNAs that encode collagens and other proteins involved in fibrosis. In this study we assessed the effects of swimming training (ST) on expression of the cardiac miRNA-29 family and on genes encoding collagen after MI in rats. METHODS: ST consisted of 60 min/day/10 weeks and began four weeks after MI. MiRNA and collagen expression analysis were performed in the infarcted region (IR), border region (BR) of the infarcted region and in the remote myocardium (RM) of the left ventricle. RESULTS: MiRNA-29a expression increased 32% in BR and 52% in RM in the TR-INF compared with SED-INF. MiRNA-29c increased by 63% in BR and 55% in RM in TR-INF compared with SED-INF group. COL IAI and COL IIIAI decreased by 63% and 62% in TR-INF, respectively, compared with SED-INF. COLIIIAI expression decreased by 16% in TR-INF compared with SED-INF. CONCLUSION: Altogether, our results showed that ST restores cardiac miRNA-29 (a and c) levels and prevents COL IAI and COL IIIAI expression in BR and RM, which may contribute to the improvement in ventricular function induced by swimming training, after MI. © 2014 S. Karger AG, Basel.


Assuntos
Colágeno/biossíntese , Regulação da Expressão Gênica , MicroRNAs/biossíntese , Infarto do Miocárdio/metabolismo , Miocárdio/metabolismo , Condicionamento Físico Animal , Natação , Animais , Masculino , Infarto do Miocárdio/patologia , Miocárdio/patologia , Ratos , Ratos Wistar
9.
Biochem Biophys Res Commun ; 441(4): 713-9, 2013 Nov 29.
Artigo em Inglês | MEDLINE | ID: mdl-24211212

RESUMO

We tested the hypothesis that AT1R blockade modulates the shear stress-induced (SS) synthesis of nitric oxide (NO) in endothelial cells (EC). The AT1R blocker Candesartan in the absence of the ligand angiotensin II (ang II) potentiated SS-induced NO synthesis accompanied by increased p-eNOS(Ser1177) and decreased p-eNOS(Thr495). Candesartan also inhibited SS-induced ERK activation and increased intracellular calcium transient in a time-dependent manner. To confirm the role of ERK to modulate p-eNOS(Thr495) and calcium to modulate p-eNOS(Ser1177), the MEK inhibitor U0126 and the calcium chelator BAPTA-AM were used, respectively. Pre-treatment of EC with U0126 completed abrogated basal and SS-induced ERK activation, inhibited p-eNOS(Thr495) and increased NO production by SS. On the other hand, pre-treatment of EC with BAPTA-AM decreased the effects of SS alone or in combination with Candesartan to induce p-eNOS(Ser1177) and partially inhibited the effects of Candesartan to potentiate NO release by SS. The AT1R blockers Losartan and Telmisartan were also tested but only Telmisartan potentiated NO synthesis and blocked SS-induced AT1R activation. Altogether, we provide evidence that Candesartan and Telmisartan potentiate SS-induced NO production even in the absence of the ligand ang II. This response requires both the inhibition of eNOS phosphorylation at its inhibitory residue Thr(495) as well as the increase of eNOS phosphorylation at its excitatory residue Ser(1177). In addition, the response is associated with inhibition of SS-induced ERK activation as well as increasing intracellular calcium transient. One may speculate that these yet undescribed events may contribute to the benefits of ARBs in cardiovascular diseases.


Assuntos
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia , Benzimidazóis/farmacologia , Células Endoteliais/efeitos dos fármacos , Óxido Nítrico Sintase Tipo III/metabolismo , Óxido Nítrico/biossíntese , Receptor Tipo 1 de Angiotensina/metabolismo , Estresse Mecânico , Tetrazóis/farmacologia , Benzoatos/farmacologia , Cálcio/metabolismo , Linhagem Celular Tumoral , Células Endoteliais/metabolismo , Ativação Enzimática , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Humanos , Fosforilação/efeitos dos fármacos , Serina/genética , Serina/metabolismo , Resistência ao Cisalhamento , Telmisartan , Treonina/genética , Treonina/metabolismo
10.
Biochem Biophys Res Commun ; 434(3): 647-52, 2013 May 10.
Artigo em Inglês | MEDLINE | ID: mdl-23583236

RESUMO

Mechanotransduction enables cells to sense and respond to stimuli, such as strain, pressure and shear stress (SS), critical for maintenance of cardiovascular homeostasis or pathological states. The angiotensin II type 1 receptor (AT1R) was the first G protein-coupled receptor described to display stretch-induced activation in cardiomyocytes independent of its ligand Ang II. Here, we assessed whether SS (15 dynes/cm(2), 10 min), an important mechanical force present in the cardiovascular system, activates AT1R independent of its ligand. SS induced extracellular signal-regulated kinase (ERK) activation, used as a surrogate of AT1R activation, in Chinese hamster ovary cells expressing the AT1R (CHO+AT1) but not in wild type cells (CHO). AT1R dependent SS-induced ERK activation involves Ca(2+) inflow and activation of Gαq since Ca(2+) chelator EGTA or Gαq-specific inhibitor YM-254890 decreased SS-induced ERK activation. On the other hand, the activation of JAK-2 and Src, two intracellular signaling molecules independent of G protein activation, were not differently modulated in the presence of AT1R. Also, ERK activation by SS was observed in CHO cells expressing the mutated AT1R DRY/AAY, which has impaired ability to activate Gαq dependent intracellular signaling. Altogether we provided evidence that SS activates AT1R in the absence of its ligand by both a G protein-dependent and -independent pathways. The biological relevance of these observations deserves to be further investigated since the novel mechanisms described extend the knowledge of the activation of GPCRs independent of its traditional ligand.


Assuntos
Proteínas de Ligação ao GTP/fisiologia , Receptor Tipo 1 de Angiotensina/metabolismo , Estresse Fisiológico , Animais , Western Blotting , Células CHO , Cricetinae , Cricetulus , Ativação Enzimática , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Reação em Cadeia da Polimerase
11.
J Physiol ; 588(Pt 13): 2431-42, 2010 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-20442263

RESUMO

Myocardial hypertrophy and dysfunction occur in response to excessive catecholaminergic drive. Adverse cardiac remodelling is associated with activation of proinflammatory cytokines in the myocardium. To test the hypothesis that exercise training can prevent myocardial dysfunction and production of proinflammatory cytokines induced by beta-adrenergic hyperactivity, male Wistar rats were assigned to one of the following four groups: sedentary non-treated (Con); sedentary isoprenaline treated (Iso); exercised non-treated (Ex); and exercised plus isoprenaline (Iso+Ex). Echocardiography, haemodynamic measurements and isolated papillary muscle were used for functional evaluations. Real-time RT-PCR and Western blot were used to quantify tumour necrosis factor alpha, interleukin-6, interleukin-10 and transforming growth factor beta(1) (TGF-beta(1)) in the tissue. NF-B expression in the nucleus was evaluated by immunohistochemical staining. The Iso rats showed a concentric hypertrophy of the left ventricle (LV). These animals exhibited marked increases in LV end-diastolic pressure and impaired myocardial performance in vitro, with a reduction in the developed tension and maximal rate of tension increase and decrease, as well as worsened recruitment of the Frank-Starling mechanism. Both gene and protein levels of tumour necrosis factor alpha and interleukin-6, as well as TGF-beta(1) mRNA, were increased. In addition, the NF-B expression in the Iso group was significantly raised. In the Iso+Ex group, the exercise training had the following effects: (1) it prevented LV hypertrophy; (ii) it improved myocardial contractility; (3) it avoided the increase of proinflammatory cytokines and improved interleukin-10 levels; and (4) it attenuated the increase of TGF-beta(1) mRNA. Thus, exercise training in a model of beta-adrenergic hyperactivity can avoid the adverse remodelling of the LV and inhibit inflammatory cytokines. Moreover, the cardioprotection is related to beneficial effects on myocardial performance.


Assuntos
Cardiomiopatias/prevenção & controle , Cardiomiopatias/fisiopatologia , Citocinas/metabolismo , Condicionamento Físico Animal/fisiologia , Receptores Adrenérgicos beta/fisiologia , Agonistas Adrenérgicos beta/farmacologia , Animais , Western Blotting , Cardiomegalia/induzido quimicamente , Cardiomegalia/fisiopatologia , Cardiomiopatias/induzido quimicamente , Cardiotônicos/farmacologia , Circulação Coronária/fisiologia , Ecocardiografia , Imuno-Histoquímica , Inflamação/metabolismo , Isoproterenol/farmacologia , Masculino , Contração Miocárdica/fisiologia , Miocárdio/metabolismo , NF-kappa B/biossíntese , Ratos , Ratos Wistar , Receptores Adrenérgicos beta/efeitos dos fármacos , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fator de Necrose Tumoral alfa/metabolismo , Função Ventricular Esquerda/fisiologia
12.
J Physiol Anthropol ; 29(1): 1-12, 2010.
Artigo em Inglês | MEDLINE | ID: mdl-20453428

RESUMO

To evaluate the effects of heat acclimation on sweat rate redistribution and thermodynamic parameters, 9 tropical native volunteers were submitted to 11 days of exercise-heat exposures (40+/-0 degrees C and 45.1+/-0.2% relative humidity). Sudomotor function was evaluated by measuring total and local (forehead, chest, arm, forearm, and thigh) sweat rates, local sweat sodium concentration, and mean skin and rectal temperatures. We also calculated heat production (H), heat storage (S), heat exchange by radiation (R) and by convection (C), evaporated sweat (E(sw)), sweating efficiency (eta(sw)), skin wettedness (w(sk)), and the ratio between the heat storage and the sum of heat production and heat gains by radiation and convection (S/(H+R+C)). The heat acclimation increased the whole-body sweat rate and reduced the mean skin temperature. There were changes in the local sweat rate patterns: on the arm, forearm, and thigh it increased significantly from day 1 to day 11 (all p<0.05) and the sweat rates from the forehead and the chest showed a small nonsignificant increase (p=0.34 and 0.17, respectively). The relative increase of local sweat rates on day 11 was not different among the sites; however, when comparing the limbs (arm, forearm, and thigh) with the trunk (forehead and chest), there was a significant higher increase in the limbs (32+/-5%) in comparison to the trunk (11+/-2%, p=0.001). After the heat acclimation period we observed higher w(sk) and E(sw) and reduced S/(H+R+C), meaning greater thermoregulatory efficiency. The increase in the limb sweat rate, but not the increase in the trunk sweat rate, correlated with the increased w(sk), E(sw), and reduced S/(H+R+C) (p<0.05 to all). Altogether, it can be concluded that heat acclimation increased the limbs' sweat rates in tropical natives and that this increase led to increased loss of heat through evaporation of sweat and this higher sweat evaporation was related to higher thermoregulatory efficiency.


Assuntos
Aclimatação/fisiologia , Temperatura Alta , Sudorese/fisiologia , Adulto , Análise de Variância , Temperatura Corporal , Brasil , Exercício , Frequência Cardíaca , Humanos , Masculino , Consumo de Oxigênio/fisiologia , Termodinâmica , Clima Tropical
13.
J Renin Angiotensin Aldosterone Syst ; 10(1): 15-23, 2009 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-19286754

RESUMO

INTRODUCTION: This study addressed the role of the local renin-angiotensin system (RAS) in the left ventricular hypertrophy (LVH) induced by swimming training using pharmacological blockade. MATERIALS AND METHODS: Female Wistar rats treated with enalapril maleate (60 mg.kg(-1).d( -1), n=38), losartan (20 mg.kg(-1).d(-1), n=36) or high salt diet (1% NaCl, n=38) were trained by two protocols (T1: 60-min swimming session, 5 days per week for 10 weeks and T2: the same T1 protocol until the 8(th) week, then 9(th) week they trained twice a day and 10(th) week they trained three times a day). Salt loading prevented activation of the systemic RAS. Haemodynamic parameters, soleus citrate synthase (SCS) activity and LVH (left ventricular/body weight ratio, mg/g) were evaluated. RESULTS: Resting heart rate decreased in all trained groups. SCS activity increased 41% and 106% in T1 andT2 groups, respectively. LVH was 20% and 30% in T1 andT2 groups, respectively. Enalapril prevented 39% of the LVH in T2 group (p<0.05). Losartan prevented 41% in T1 and 50% inT2 (p<0.05) of the LVH in trained groups. Plasma renin activity (PRA) was inhibited in all salt groups and it was increased in T2 group. CONCLUSIONS: These data provide evidence that the physiological LVH induced by swimming training is regulated by local RAS independent from the systemic, because the hypertrophic response was maintained even when PRA was inhibited by chronic salt loading. However, other systems can contribute to this process.


Assuntos
Anti-Hipertensivos/farmacologia , Hipertrofia Ventricular Esquerda/sangue , Hipertrofia Ventricular Esquerda/fisiopatologia , Condicionamento Físico Animal , Sistema Renina-Angiotensina/efeitos dos fármacos , Renina/sangue , Natação/fisiologia , Animais , Peso Corporal/efeitos dos fármacos , Citrato (si)-Sintase/metabolismo , Feminino , Hemodinâmica/efeitos dos fármacos , Hipertrofia Ventricular Esquerda/enzimologia , Hipertrofia Ventricular Esquerda/patologia , Tamanho do Órgão/efeitos dos fármacos , Ratos , Ratos Wistar , Sistema Renina-Angiotensina/fisiologia
14.
Am J Physiol Regul Integr Comp Physiol ; 295(2): R381-7, 2008 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-18495827

RESUMO

Resistance training is accompanied by cardiac hypertrophy, but the role of the renin-angiotensin system (RAS) in this response is elusive. We evaluated this question in 36 male Wistar rats divided into six groups: control (n=6); trained (n=6); control+losartan (10 mg.kg(-1).day(-1), n=6); trained+losartan (n=6); control+high-salt diet (1%, n=6); and trained+high-salt diet (1%, n=6). High salt was used to inhibit the systemic RAS and losartan to block the AT1 receptor. The exercise protocol consisted of: 4x12 bouts, 5x/wk during 8 wk, with 65-75% of one repetition maximum. Left ventricle weight-to-body weight ratio increased only in trained and trained+high-salt diet groups (8.5% and 10.6%, P<0.05) compared with control. Also, none of the pathological cardiac hypertrophy markers, atrial natriuretic peptide, and alphaMHC (alpha-myosin heavy chain)-to-betaMHC ratio, were changed. ACE activity was analyzed by fluorometric assay (systemic and cardiac) and plasma renin activity (PRA) by RIA and remained unchanged upon resistance training, whereas PRA decreased significantly with the high-salt diet. Interestingly, using Western blot analysis and RT-PRC, no changes were observed in cardiac AT2 receptor levels, whereas the AT1 receptor gene (56%, P<0.05) and protein (31%, P<0.05) expressions were upregulated in the trained group. Also, cardiac ANG II concentration evaluated by ELISA remained unchanged (23.27+/-2.4 vs. 22.01+/-0.8 pg/mg, P>0.05). Administration of a subhypotensive dose of losartan prevented left ventricle hypertrophy in response to the resistance training. Altogether, we provide evidence that resistance training-induced cardiac hypertrophy is accompanied by induction of AT1 receptor expression with no changes in cardiac ANG II, which suggests a local activation of the RAS consistent with the hypertrophic response.


Assuntos
Hipertrofia Ventricular Esquerda/metabolismo , Miocárdio/metabolismo , Esforço Físico , Receptor Tipo 1 de Angiotensina/metabolismo , Sistema Renina-Angiotensina , Adaptação Fisiológica , Angiotensina II/metabolismo , Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia , Animais , Western Blotting , Peso Corporal , Modelos Animais de Doenças , Ensaio de Imunoadsorção Enzimática , Hemodinâmica , Hipertrofia Ventricular Esquerda/fisiopatologia , Hipertrofia Ventricular Esquerda/prevenção & controle , Losartan/farmacologia , Masculino , Força Muscular , Miocárdio/patologia , Reação em Cadeia da Polimerase , RNA Mensageiro/metabolismo , Ratos , Ratos Wistar , Receptor Tipo 1 de Angiotensina/efeitos dos fármacos , Receptor Tipo 1 de Angiotensina/genética , Receptor Tipo 2 de Angiotensina/metabolismo , Sistema Renina-Angiotensina/efeitos dos fármacos , Cloreto de Sódio na Dieta/administração & dosagem , Regulação para Cima
15.
Clin Exp Pharmacol Physiol ; 32(4): 249-54, 2005 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-15810987

RESUMO

1. The present study sought to evaluate cardiovascular adaptations, such as blood pressure (BP), heart rate (HR) and cardiac hypertrophy, to resistance training (RT) in a rat model. 2. The training protocol consisted of four sets of 10-12 repetitions of the squat exercise performed at 65-75% of one repetition maximum (1RM) over 4 weeks. Animals were randomly divided into three groups: control (n = 8, CO), electrically stimulated (n = 8, ES) and trained (n = 8, TR; also electrically stimulated). Blood pressure and HR were measured by a direct method in conscious rats after the training period. 3. All groups began with similar 1RM and 1RM/bodyweight (BW) ratio, however, at the end of the protocol only the TR group was different from the beginning (56% and 50%, respectively; both P < 0.01). The CO and ES groups had similar values for cardiac chambers weight/BW ratio, HR and diastolic, systolic and mean BP. Left ventricular hypertrophy (LVH) determined by the left ventricle (LV) weight/BW ratio was increased in the TR group (12%) when compared to CO (P < 0.01) or ES groups (P < 0.01). No changes were found in the weights of the atrium or right ventricle. Diastolic (14%) and mean BP (13%) were lower in the TR group (P < 0.05), whereas systolic BP and HR remained unchanged. 4. Collectively these results demonstrate that the rat RT model used is associated with significant development of cardiac hypertrophy and lowering of resting BP. These cardiovascular adaptations seem to a result of the training exercise and not influenced by stress since circulating catecholamine levels and adrenal gland weights remained unchanged in all groups.


Assuntos
Fenômenos Fisiológicos Cardiovasculares , Condicionamento Físico Animal/fisiologia , Glândulas Suprarrenais/anatomia & histologia , Animais , Pressão Sanguínea/fisiologia , Peso Corporal/fisiologia , Catecolaminas/sangue , Estimulação Elétrica , Coração/anatomia & histologia , Modelos Animais , Músculo Esquelético/anatomia & histologia , Músculo Esquelético/fisiologia , Tamanho do Órgão/fisiologia , Distribuição Aleatória , Ratos , Ratos Wistar , Levantamento de Peso/fisiologia , Suporte de Carga/fisiologia
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