Abstract

Background: Angiotensin-(1-7) [Ang-(1-7)] plays a counterregulatory role to Ang II in renin angiotensin system such as antihypertension, antihypertrophy, and antifibrosis. In trained spontaneous hypertensive (HTN) rats, Mas expression and protein are upregulated in ventricular tissue. Therefore, we hypothesized that Ang-(1-7) has effects on hemodynamics, cardiac function and cardiac remodeling in trained two-kidney, one-clip (2K1C) hypertensive rats. The objective of present study was to investigate the role of Ang-(1-7) on cardiac hemodynamics, cardiac function and cardiac remodeling in trained 2K1C hypertensive rats. Materials and Methods: Rats were divided into sedentary and trained groups. Each group consists of sham, 2K1C rats and 2K1C rats with Ang-(1-7) infusion. Swimming training was performed for 1 hr/day, 5 days/wk for 4 wks following 1 wk swimming training for acclimatization. Angiotensin-(1-7), at a dose of 576ug/kg/day via mini-osmotic pump, was infused. Blood pressure measurement, echocardiographic measurement, radioimmunoassay of plasma ANP, hematoxylin, and trichrome staining were performed. Mas protein was evaluated using western blotting. Results: 2K1C rats showed moderate hypertension and left ventricular hypertrophy without changing left ventricular function. Chronic Ang-(1-7) infusion attenuated hypertension and cardiac hypertrophy only in trained 2K1C rats but not in sedentary 2K1C rats. Chronic Ang-(1-7) treatment significantly decreased ventricular myocyte diameter and cardiac fibrosis in only trained 2K1C rats. Chronic Ang-(1-7) treatment had no effect on left ventricular function. The Mas protein level in ventricle was up-regulated in trained 2K1C rats. Conclusions: In conclusion, chronic Ang-(1-7) infusion attenuates hypertension and cardiac remodeling in trained 2K1C rats probably via upregulation of Mas receptor.

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