Navegando por Palavras-chave "angiotensina II"

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    The effect of hypoxia and reoxygenation in the response of mesangial cells to angiotensin II in vitro
    (Sociedade Brasileira de Nefrologia, 2013-12-01) Razvickas, Clara Versolato [UNIFESP]; Borges, Fernanda Teixeira [UNIFESP]; Oliveira, Andréia Silva De [UNIFESP]; Schor, Nestor [UNIFESP]; Boim, Mirian Aparecida [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    INTRODUCTION: Mesangial cells (MC) may be involved in the glomerular alterations induced by ischemia/reperfusion injury. OBJECTIVE: To evaluate the response of immortalized MC (IMC) to 30 minutes of hypoxia followed by reoxygenation periods of 30 minutes (H/R30) or 24 hours (H/R24). METHODS: The intracellular calcium concentration ([Ca+2]i) was measured before (baseline) and after adding angiotensin II (AII, 10-5 M) in the presence and absence of glybenclamide (K ATP channel blocker). We estimated the level of intracellular ATP, nitric oxide (NO) and PGE2. RESULTS: ATP concentration decreased after hypoxia and increased after reoxygenation. Hypoxia and H/R induced increases in basal [Ca+2]i. AII induced increases in [Ca+2]i in normoxia (97 ± 9%), hypoxia (72 ± 10%) or HR30 (85 ± 17%) groups, but there was a decrease in the response to AII in group H/R24 since the elevation in [Ca+2]i was significantly lower than in control (61 ± 10%, p < 0.05). Glybenclamide did not modify this response. It was observed a significant increase in NO generation after 24 hours of reoxygenation, but no difference in PGE2 production was observed. Data suggest that H/R injury is characterized by increased basal [Ca+2]i and by an impairment in the response of cells to AII. Results suggest that the relative insensibility to AII may be at least in part mediated by NO but not by prostaglandins or vasodilator K ATP channels. CONCLUSION: H/R caused dysfunction in IMC characterized by increases in basal [Ca+2]i during hypoxia and reduction in the functional response to AII during reoxygenation.
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    Elastase-2, a Tissue Alternative Pathway for Angiotensin II Generation, Plays a Role in Circulatory Sympathovagal Balance in Mice
    (Frontiers Media Sa, 2017) Becari, Christiane; Durand, Marina T.; Guimaraes, Alessander O. [UNIFESP]; Lataro, Renata M.; Prado, Cibele M.; de Oliveira, Mauro; Candido, Sarai C. O.; Pais, Paloma; Ribeiro, Mauricio S.; Bader, Michael; Pesquero, Joao B. [UNIFESP]; Salgado, Maria C. O.; Salgado, Helio C.
    In vitro and ex vivo experiments indicate that elastase-2 (ELA-2), a chymotrypsin-serine protease elastase family member 2A, is an alternative pathway for angiotensin II (Ang II) generation. However, the role played by ELA-2 in vivo is unclear. We examined ELA-2 knockout (ELA-2K0) mice compared to wild-type (WT) mice and determined whether ELA-2 played a role in hemodynamics [arterial pressure (AP) and heart rate (HR)], cardiocirculatory sympathovagal balance and baroreflex sensitivity. The variability of systolic arterial pressure (SAP) and pulse interval (PI) for evaluating autonomic modulation was examined for time and frequency domains (spectral analysis), whereas a symbolic analysis was also used to evaluate PI variability. In addition, baroreflex sensitivity was examined using the sequence method. Cardiac function was evaluated echocardiographically under anesthesia. The AP was normal whereas the HR was reduced in ELA-2K0 mice (425 +/- 17 vs. 512 +/- 13 bpm from WT). SAP variability and baroreflex sensitivity were similar in both strains. The LF power from the PI spectrum (33.6 +/- 5 vs. 51.8 +/- 4.8 nu from WT) and the LF/HF ratio (0.60 +/- 0.1 vs. 1.45 +/- 0.3 from WT) were reduced, whereas the HF power was increased (66.4 +/- 5 vs. 48.2 +/- 4.8 nu from WI) in ELA-2K0 mice, indicating a shift toward parasympathetic modulation of HR. Echocardiographic examination showed normal fractional shortening and an ejection fraction in ELA-2K0 mice