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ACE and iNOS overexpression correlates with vascular reactivity in young Syrian cardiomyopathic hamsters (1075.7)
Author(s) -
Cruz Nildris,
Quidgley Jose,
Dorna Luisamari,
Miranda Jorge,
Crespo Maria
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1075.7
Subject(s) - enos , medicine , western blot , messenger rna , endocrinology , syrian hamsters , downregulation and upregulation , heart failure , biology , nitric oxide synthase , nitric oxide , hamster , biochemistry , gene
Vascular alterations are present in 2‐month‐old Syrian cardiomyopathic hamsters (SCH) before the clinical manifestation of HF. Aortic ACE, eNOS, and iNOS mRNA and protein levels were assessed in SCH from 1 to 4 months of age to elucidate the timeframe and the mechanisms underlying these alterations. Total RNA and proteins were extracted from aortas, and quantified with Real‐Time RT‐PCR and Western blot. ACE mRNA and protein were upregulated in 2‐month‐old SCH by 41% and 43%, respectively, when compared to control (CT; P<0.05). Protein levels of iNOS were higher in SCH (482%) than in CT (100%) at 2 months of age. In addition, eNOS mRNA increased by 77% in SCH, whereas eNOS protein levels were 15% lower in SCH than in CT (P<0.05). These findings suggest that the vascular reactivity present in 2‐month‐old SCH is secondary to overactivation of RAS resulting from increased levels of ACE mRNA and protein. A combination of lower eNOS and higher iNOS protein levels may underlie endothelial dysfunction present in SCH at this stage. Altogether, these factors will likely promote vascular hyper‐reactivity in the early stages of heart failure in SCH and eventually trigger cardiac deterioration. Grant Funding Source : Supported by MBRS‐RISE R25‐GM061838