Decreased cardiac Ang-(1-7) is associated with salt-induced cardiac remodeling and dysfunction

The adverse cardiac effects of excessive salt intake may result not only from the undesirable action of angiotensin II but may also be a consequence of diminished protective effects of the angiotensin-(1-7).

Eight-week-old male spontaneously hypertensive rats (SHR) were given an 8% salt diet for 5 weeks (n = 8). Age- and gender-matched controls received standard chow (n = 6).

Angiotensin II has a critical role in the regulation of blood pressure and cell growth and excess activity of the peptide is implicated in the pathogenesis of salt-induced cardiovascular injury. On the other hand, the role of counteracting angiotensin-(1-7) in cardiac structural and functional responses to high salt diet has not been elucidated. Therefore, the present study examined the changes in cardiac angiotensin-(1-7), its forming enzyme angiotensin converting enzyme 2 (ACE2) and receptor mas in response to a high salt diet in spontaneously hypertensive rats (SHR).

Salt excess increased arterial pressure (p < 0.05) and plasma renin and angiotensin II concentrations (p < 0.05). Salt-induced left ventricular remodeling and diastolic dysfunction were associated with diminished levels of angiotensin-(1-7) in the heart (p < 0.05) and no changes in cardiac angiotensin II levels. Exposure to high salt intake decreased cardiac ACE2 mRNA and protein level (p < 0.05). There was no difference in the protein levels of angiotensin II type 1 and mas receptors between the two experimental groups.