Premium
High salt diet reduced cardiac angiotensin‐(1‐7) but not ACE2 activity in SHR
Author(s) -
Varagic Jasmina,
Brosnihan K. Bridget,
Chappell Mark C.,
Ferrario Carlos M.
Publication year - 2009
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.23.1_supplement.626.22
Subject(s) - medicine , endocrinology , angiotensin ii , cardiac hypertrophy , cardiac fibrosis , renin–angiotensin system , dietary salt , left ventricular hypertrophy , muscle hypertrophy , fibrosis , blood pressure
Despite numerous studies suggesting that angiotensin‐(1‐7) [Ang‐(1‐7)] counterbalances the biological actions of angiotensin II (Ang II), little is known about its response in salt‐induced left ventricular (LV) remodeling. Thus, we examined whether an inadequate balance between these peptides might contribute to the previously shown LV hypertrophic and proliferative response to high dietary salt intake in spontaneously hypertensive rats (SHR) ( Varagic, AJP 2008 ). Eight week‐old male SHR were given an 8% salt diet for 5 weeks (Salt; n=8) and age‐matched controls received standard chow (Control; n=6). Increased salt intake exaggerated hypertension (221 ± 10 mm Hg) compared to rats given a normal salt diet (188 ± 9 mmHg) and aggravated cardiac hypertrophy and fibrosis. Although LV tissue Ang II content was not changed, high dietary salt intake reduced the cardiac content of Ang‐(1‐7) as well as Ang‐(1‐7)/Ang II ratio (Figure). Despite the reduction in Ang‐(1‐7), salt excess did not influence cardiac ACE2 activity (Salt: 21.01 ± 2.05 vs. Control: 22.25 ± 1.55 fmol/mg/min). In conclusion, the significant reduction in the cardiac content of Ang‐(1‐7) in response to a high salt diet suggests a critical role for the peptide in the development of salt‐related cardiac remodeling. The inability to increase ACE2 suggests that other enzymes may affect Ang‐(1‐7) metabolism under the conditions of dietary salt excess.