Browsing by Author "Jalil, Jorge E."

Now showing 1 - 6 of 6
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    Angiotensin-(1-9) regulates cardiac hypertrophy in vivo and in vitro
    (LIPPINCOTT WILLIAMS & WILKINS, 2010) Paz Ocaranza, Maria; Lavandero, Sergio; Jalil, Jorge E.; Moya, Jaqueline; Pinto, Melissa; Novoa, Ulises; Apablaza, Felipe; Gonzalez, Leticia; Hernandez, Carol; Varas, Manuel; Lopez, Rene; Godoy, Ivan; Verdejo, Hugo; Chiong, Mario
    Background Angiotensin-(1-9) is present in human and rat plasma and its circulating levels increased early after myocardial infarction or in animals treated with angiotensin-converting enzyme inhibitor. However, the cardiovascular effects of this peptide are unknown.
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    Enalapril attenuates downregulation of angiotensin-converting enzyme 2 in the late phase of ventricular dysfunction in myocardial infarcted rat
    (LIPPINCOTT WILLIAMS & WILKINS, 2006) Ocaranza, Maria Paz; Godoy, Ivan; Jalil, Jorge E.; Varas, Manuel; Collantes, Patricia; Pinto, Melissa; Roman, Maritza; Ramirez, Cristian; Copaja, Miguel; Diaz Araya, Guillermo; Castro, Pablo; Lavandero, Sergio
    The early and long-term effects of coronary artery ligation on the plasma and left ventricular angiotensin-converting enzyme (ACE and ACE2) activities, ACE and ACE2 mRNA levels, circulating angiotensin (Ang) levels [Ang I, Ang-(1-7), Ang-(1-9), and Ang II], and cardiac function were evaluated 1 and 8 weeks after experimental myocardial infarction in adult Sprague Dawley rats. Sham-operated rats were used as controls. Coronary artery ligation caused myocardial infarction, hypertrophy, and dysfunction 8 weeks after surgery. At week 1, circulating Ang II and Ang-(1-9) levels as well as left ventricular and plasma ACE and ACE2 activities increased in myocardial-infarcted rats as compared with controls. At 8 weeks post-myocardial infarction, circulating ACE activity, ACE mRNA levels, and Ang II levels remained higher, but plasma and left ventricular ACE2 activities and mRNA levels and circulating levels of Ang-(1-9) were lower than in controls. No changes in plasma Ang-(1-7) levels were observed at any time. Enalapril prevented cardiac hypertrophy and dysfunction as well as the changes in left ventricular ACE, left ventricular and plasmatic ACE2, and circulating levels of Ang II and Ang-(1-9) after 8 weeks postinfafction. Thus, the decrease in ACE2 expression and activity and circulating Ang-(1-9) levels in late ventricular dysfunction post-myocardial infarction were prevented with enalapril. These findings suggest that in this second arm of the renin-angiotensin system, ACE2 may act through Ang-(1-9), rather than Ang-(1-7), as a counterregulator of the first arm, where ACE catalyzes the formation of Ang II.
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    Hipertrofia cardiaca: eventos moleculares y celulares
    (2006) Carreño, Juan Eduardo; Apablaza, Felipe; Ocaranza, María Paz; Jalil, Jorge E.
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    Left cardiac remodelling assessed by echocardiography is associated with rho-kinase activation in long-distance runners
    (Wiley, 2021) Contreras Briceño, Felipe; Vega, Julián; Mandiola, Jorge; Ocaranza, María Paz; Herrera, Sebastián; Salinas, Manuel; Fernández, Rodrigo; Jalil, Jorge E.; Lavandero, Sergio; Chiong, Mario; Godoy, Paz; Castro, Pablo F.; Sitges, Marta; Gabrielli, Luigi
    This single-blind and cross-sectional study evaluated the role of Rho-kinase (ROCK) as a biomarker of the cardiovascular remodelling process assessed by echocardiography in competitive long-distance runners (LDRs) during the training period before a marathon race. Thirty-six healthy male LDRs (37.0 ± 5.3 years; 174.0 ± 7.0 height; BMI: 23.8 ± 2.8;.V O2-peak: 56.5 ± 7.3 mL·kg−1·min−1) were separated into two groups according to previous training level: high-training (HT, n = 16) ≥ 100 km·week−1 and low-training (LT, n = 20) ≥ 70 and < 100 km·week−1. Also, twenty-one healthy nonactive subjects were included as a control group (CTR). A transthoracic echocardiography was performed and ROCK activity levels in circulating leukocytes were measured at rest (48 h without exercising) the week before the race. The HT group showed a higher left ventricular mass index (LVMi) and left atrial volume index (LAVi) than other groups (p < 0.05, for both); also, higher levels of ROCK activity were found in LDRs (HT = 6.17 ± 1.41 vs. CTR = 1.64 ± 0.66 (p < 0.01); vs. LT = 2.74 ± 0.84; (p < 0.05)). In LDRs a direct correlation between ROCK activity levels and LVMi (r = 0.83; p < 0.001), and LAVi (r = 0.70; p < 0.001) were found. In conclusion, in male competitive long-distance runners, the load of exercise implicated in marathon training is associated with ROCK activity levels and the left cardiac remodelling process assessed by echocardiography.
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    Markedly increased Rho-kinase activity in circulating leukocytes in patients with chronic heart failure
    (MOSBY-ELSEVIER, 2011) Paz Ocaranza, Maria; Gabrielli, Luigi; Mora, Italo; Garcia, Lorena; McNab, Paul; Godoy, Ivan; Braun, Sandra; Cordova, Samuel; Castro, Pablo; Novoa, Ulises; Chiong, Mario; Lavandero, Sergio; Jalil, Jorge E.
    Background The small guanosine triphosphatase Rho and its target Rho-kinase have significant roles in experimental remodeling and ventricular dysfunction, but no data are available on Rho-kinase activation in patients with heart failure (HF). We hypothesized that, in patients with chronic HF, Rho-kinase in circulating leukocytes is activated and related to left ventricular (LV) remodeling and dysfunction.
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    Osmotically-induced genes are controlled by the transcription factor TonEBP in cultured cardiomyocytes
    (ACADEMIC PRESS INC ELSEVIER SCIENCE, 2008) Navarro, Paola; Chiong, Mario; Volkwein, Karen; Moraga, Francisco; Ocaranza, Maria Paz; Jalil, Jorge E.; Lim, Sun Woo; Kim, Jeong Ah; Kwon, H. Moo; Lavandero, Sergio
    Changes in cardiac osmolarity occur in myocardial infarction. Osmoregulatory mechanism may, therefore, play a Crucial role in cardiomyocyte survival. Tonicity-responsive enhancer binding protein (TonEBP) is a key transcription factor participating in the adaptation of cells to increases in tonicity. However, it is unknown whether cardiac TonEBP is activated by tonicity. Hypertonicity activated transcriptional activity of TonEBP, increased the amounts of both TonEBP mRNA and protein, and induced both the mRNA and protein of TonEBP target genes (aldose reductase and heat shock protein-70). Hypotonicity decreased the amount of TonEBP protein indicating bidirectional osmoregulation of this transcription factor. Adenoviral expression of a dominant negative TonEBP suppressed the hypertonicity-dependent increase of aldose reductase protein. These results indicated that TonEBP controls osmoregulatory mechanisms in cardiomyocytes. (C) 2008 Elsevier Inc. All rights reserved.