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Renal Function of Rats with Isoproternol‐induced Cardiac Hypertrophy
Author(s) -
Thieme Karina,
OliveiraSouza Maria
Publication year - 2010
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.24.1_supplement.1059.20
Subject(s) - endocrinology , medicine , renal function , renal blood flow , muscle hypertrophy , cardiac hypertrophy , cardiac function curve , chemistry , stimulation , excretion , angiotensin ii , kidney , inulin , cardiac output , western blot , receptor , hemodynamics , biochemistry , heart failure , gene
Aim Avaliate the effect of Isoproterenol‐induced cardiac hypertrophy on renal function and proteic expression in rats. Methods Male Wistar rats were submitted to subcutaneous injection of isoproterenol (ISO) (0.3 mg.kg(‐1).day(‐1) sc) or vehicle for 7 days. Renal plasmatic flow (RPF) and glomerular filtration rate (GFR) were determined by para aminohypurate and inulin clearance. The excretion of ions was also analyzed. Cardiac hypertrophy and organs congestion were evaluated by respective organs weights. The proteic expression of many renal transporters and Angiotensin II receptors will be analysed by Western Blot technique. Results and Discussion Chronic β‐adrenergic stimulation does not affect hemodynamic parameters, despite cardiac hypertrophy. Our results showed that ISO‐treatment does not affect RPF (control: 4,19 ± 0,45; n = 12 versus ISO: 4,17 ± 0,36; n = 11), which is consistent with a normal cardiac output found in this model. However, there was a significant decrease of GFR (control: 2,24 ± 0,22; n = 12 versus ISO: 1,49 ± 0,13; n = 11 * p< 0.01), which could be related to inflammatory process, leading to alteration in ultratiltration coefficient (K f ). Urinary Na + and K + were significantly reduced and enhanced, respectively. These changes in excretion of ions could be related to alterations in expression of renal transporters and are under investigation. Research Support: Fapesp