Navegando por Autor "Casali, Karina Rabello"
Agora exibindo 1 - 2 de 2
Resultados por página
Opções de Ordenação
Item An orally active angiotensin-(1–7) inclusion compound and exercisetraining produce similar cardiovascular effects in spontaneouslyhypertensive rats.(2014) Bertagnolli, Mariane; Casali, Karina Rabello; Sousa, Frederico Barros de; Rigatto, Katya; Oliveira, Lenice Kappes Becker; Santos, Sergio Henrique Sousa; Dias, Lucinara Dadda; Pinto, Graziela; Dartora, Daniela Ravizzoni; Schaan, Beatriz D'Agord; Milan, Ruben Dario Sinisterra; Irigoyen, Maria Claudia; Santos, Robson Augusto Souza dosLow angiotensin-(1–7) (Ang-(1–7)) concentration is observed in some cardiovascular diseases and exer-cise training seems to restore its concentration in the heart. Recently, a novel formulation of an orallyactive Ang-(1–7) included in hydroxy-propyl-beta-cyclodextrin (HPB-CD) was developed and chronicallyadministered in experimental models of cardiovascular diseases. The present study examined whetherchronic administration of HPB-CD/Ang-(1–7) produces beneficial cardiovascular effects in spontaneouslyhypertensive rats (SHR), as well as to compare the results obtained with those produced by exercisetraining. Male SHR (15-week old) were divided in control (tap water) or treated with HPB-CD/Ang-(1–7)(corresponding to 30 _g kg−1day−1of Ang-(1–7)) by gavage, concomitantly or not to exercise training(treadmill, 10 weeks). After chronic treatment, hemodynamic, morphometric and molecular analysis inthe heart were performed. Chronic HPB-CD/Ang-(1–7) decreased arterial blood pressure (BP) and heartrate in SHR. The inclusion compound significantly improved left ventricular (LV) end-diastolic pressure,restored the maximum and minimum derivatives (dP/dT) and decreased cardiac hypertrophy index inSHR. Chronic treatment improved autonomic control by attenuating sympathetic modulation on heartand vessels and the SAP variability, as well as increasing parasympathetic modulation and HR variability.Overall results were similar to those obtained with exercise training. These results show that chronictreatment with the HPB-CD/Ang-(1–7) inclusion compound produced beneficial effects in SHR resem-bling the ones produced by exercise training. This observation reinforces the potential cardiovasculartherapeutic effect of this novel peptide formulation.Item Chronic treatment with ivabradine does not affect cardiovascular autonomic control in rats.(2016) Silva, Fernanda Cacilda dos Santos; Paiva, Franciny Aparecida; Ribeiro, Flavia Camargos de Figueiredo Müller; Caldeira, Henrique Martins Arantes; Fontes, Marco Antônio Peliky; Menezes, Rodrigo Cunha Alvim de; Casali, Karina Rabello; Fortes, Gláucia Helena; Tobaldini, Eleonora; Solbiati, Monica; Montano, Nicola; Silva, Valdo José Dias da; Chianca Júnior, Deoclécio AlvesA low resting heart rate (HR) would be of great benefit in cardiovascular diseases. Ivabradine-a novel selective inhibitor of hyperpolarization-activated cyclic nucleotide gated (HCN) channels- has emerged as a promising HR lowering drug. Its effects on the autonomic HR control are little known. This study assessed the effects of chronic treatment with ivabradine on the modulatory, reflex and tonic cardiovascular autonomic control and on the renal sympathetic nerve activity (RSNA). Male Wistar rats were divided in 2 groups, receiving intraperitoneal injections of vehicle (VEH) or ivabradine (IVA) during 7 or 8 consecutive days. Rats were submitted to vessels cannulation to perform arterial blood pressure (AP) and HR recordings in freely moving rats. Time series of resting pulse interval and systolic AP were used to measure cardiovascular variability parameters. We also assessed the baroreflex, chemoreflex and the Bezold-Jarish reflex sensitivities. To better evaluate the effects of ivabradine on the autonomic control of the heart, we performed sympathetic and vagal autonomic blockade. As expected, ivabradine-treated rats showed a lower resting (VEH: 362 ± 16 bpm vs. IVA: 260 ± 14 bpm, p = 0.0005) and intrinsic HR (VEH: 369 ± 9 bpm vs. IVA: 326 ± 11 bpm, p = 0.0146). However, the chronic treatment with ivabradine did not change normalized HR spectral parameters LF (nu) (VEH: 24.2 ± 4.6 vs. IVA: 29.8 ± 6.4; p > 0.05); HF (nu) (VEH: 75.1 ± 3.7 vs. IVA: 69.2 ± 5.8; p > 0.05), any cardiovascular reflexes, neither the tonic autonomic control of the HR (tonic sympathovagal index; VEH: 0.91± 0.02 vs. IVA: 0.88 ± 0.03, p = 0.3494). We performed the AP, HR and RSNA recordings in urethane-anesthetized rats. The chronic treatment with ivabradine reduced the resting HR (VEH: 364 ± 12 bpm vs. IVA: 207 ± 11 bpm, p < 0.0001), without affecting RSNA (VEH: 117 ± 16 vs. IVA: 120 ± 9 spikes/s, p = 0.9100) and mean arterial pressure (VEH: 70 ± 4 vs. IVA: 77 ± 6 mmHg, p = 0.3293). Our results suggest that, in health rats, the long-term treatment with ivabradine directly reduces the HR without changing the RSNA modulation and the reflex and tonic autonomic control of the heart.