EEF- Escola de Educação Física

Permanent URI for this community

https://monog.ufop.br/handle/123456789/3658

Browse

Browsing EEF- Escola de Educação Física by Author "Alzamora, Andréia Carvalho"

Now showing 1 - 3 of 3
  • No Thumbnail Available
    Item
    Fitness is improved by adjustments in muscle intracellular signaling in rats with renovascular hypertension 2K1C undergoing voluntary physical exercise.
    (2020) Lima, Taynara Carolina; Barbosa, Maria Andréa; Costa, Daniela Caldeira; Oliveira, Lenice Kappes Becker; Cardoso, Leonardo Máximo; Alzamora, Andréia Carvalho
    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. After 4 weeks, exhaustion test, plasma lactate, cardiovascular parameters were evaluated and gastrocnemius muscle was removed for evaluation of gene expression of muscle metabolism markers (PGC1α; AMPK, SIRT-1, UCP-3; MCP-1; LDH) and of the redox process. Key findings: ExV decreased blood lactate concentration and increased SOD and CAT activity and a SIRT-1 and UCP-3 gene expression in the gastrocnemius muscle of 2K1C-ExV rats compared to 2K1C-SED rats. Gene expressions of PGC1α, UCP-3, MCT-1, AMPK were higher in 2K1C-ExV rats compared to SHAM-SED rats. Blood pressure in 2K1C-ExV was lower compared to 2K1C-SED and higher in SHAM-SED rats. Reflex bradycardia in 2K1C-EX rats increased compared to 2K1C-SED and was similar to SHAM-SED. The variation in mean blood pressure induced by ganglion blocker hexamethonium and Ang II AT1 receptor antagonist, losartan in the 2K1CExV rats was smaller compared to the 2K1C-SED rats and it was similar to the SHAM-SED rats. Significance: O ExV induced adaptive responses in 2K1C-ExV rats by decreasing sympathetic and Ang II activities and stimulating intracellular signaling that favors redox balance and reduced blood lactate concentration. These adaptive responses, then, contribute to reduced arterial pressure, improved baroreflex sensitivity and physical fitness of 2K1C rats.
  • No Thumbnail Available
    Item
    Hypotensive effect induced by microinjection of Alamandine, a derivative of angiotensin-(1–7), into caudal ventrolateral medulla of 2K1C hypertensive rats.
    (2017) Soares, Everton Rocha; Barbosa, Claudiane Maria; Santos, Maria José Campagnole dos; Santos, Robson Augusto Souza dos; Alzamora, Andréia Carvalho
    In the present study we evaluated the cardiovascular effects produced by microinjection of the new component of the renin-angiotensin system, alamandine, into caudal ventrolateral medulla of urethane-anesthetized normotensive and hypertensive 2K1C rats. The participation of different angiotensin receptors in the effects of alamandine was also evaluated. Microinjection of angiotensin-(1–7) was used for comparison. The microinjection of 4, 40 and 140 pmol of alamandine or angiotensin-(1–7) into caudal ventrolateral medulla induced similar hypotensive effects in Sham-operated rats. However, contrasting with angiotensin-(1–7), in 2K1C rats the MAP response to the highest dose of alamandine was similar to that observed with saline. The microinjection of A- 779, a selective Mas receptor antagonist, blunted the angiotensin-(1–7) effects but did not block the hypotensive effect of alamandine in Sham or in 2K1C rats. However, microinjection of D-Pro7-angiotensin-(1–7), a Mas/MrgD receptor antagonist, blocked the hypotensive effect induced by both peptides. Furthermore, microinjection of PD123319, a putative AT2 receptor antagonist blocked the hypotensive effect of alamandine, but not of angiotensin-( 1–7), in Sham and 2K1C rats. Microinjection of the AT1 receptor antagonist, losartan, did not alter the hypotensive effect of angiotensin-(1–7) or alamandine in both groups. These results provide new insights about the differential mechanisms participating in the central cardiovascular effects of alamandine and angiotensin- (1–7) in normotensive and 2K1C hypertensive rats.
  • 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.