Role of Mas receptor in renal blood flow response to angiotensin (1-7) in male and female rats

Abstract

Abstract. Epidemiologic and clinical studies have shown that progression of renal disease in male is faster than that in female. However, the exact mechanisms are not well recognized. Angiotensin (1-7) (Ang 1-7) receptor, called "Mas", is an element in the depressor arm of renin angiotensin system (RAS), and its expression is enhanced in females. We test the hypothesis that Mas receptor (MasR) blockade (A779) attenuates renal blood flow (RBF) in response to infusion of graded doses of Ang 1-7 in female rats. Male and female Wistar rats were anesthetized and catheterized. Then, the mean arterial pressure (MAP), RBF, and controlled renal perfusion pressure (RPP) responses to infusion of graded doses of Ang 1-7 (100-1000 ng/kg/min i.v) with and without A779 were measured in the animals. Basal MAP, RPP, RBF, and renal vascular resistance (RVR) were not significantly different between the two groups. After Ang 1-7 administration, RPP was controlled at a constant level. However, RBF increased in a dose-related manner in response to Ang 1-7 infusion in both male and female rats (p dose < 0.0001), but MasR blockade significantly attenuated this response only in female (p group = 0.04) and not male (p group = 0.23). In addition, A779 increased the RBF response to Ang 1-7 to a greater extent. This is while the increase in male was not significant when compared with that in female (p gender = 0.08). RVR response to Ang 1-7 was insignificantly attenuated by A779 in both genders. The MasR differently regulated RBF response to Ang 1-7 in the two genders, and the effect was greater in female rats. The MasR may be a target for improvement of kidney circulation in renal diseases.

Endotoxin-induced skeletal muscle wasting is prevented by angiotensin-(1–7) through a p38 MAPK-dependent mechanism

“…In the present study we used male mice to evaluate the effect of Ang-(1-7) on LPS-induced muscle wasting; however, there is evidence that indicates sex-dependent differences in: (i) muscle composition and its functionality [51,52]; (ii) prognosis in sepsis [53,54]; and (iii) the expression and activation of the Ang-(1-7)/Mas receptor axis in cardiovascular pathologies [55][56][57][58]. For this reason, further studies could be performed in female mice to elucidate the different sex-related response to Ang-(1-7) on muscle wasting induced by LPS.…”

Renoprotective impact of angiotensin 1-7: Is it certain?

“…Moreover, by inhibition of AngII receptors (AT1R and AT2R) and Ang1-7 receptor (MasR), the RBF response to Ang1-7 infusion increased in male (not in female) (34). These results bring a conclusion that RBF response to Ang1-7 may exert via different pathways from the MasR line (33,34). We also reported before, when MasR was blocked, the RBF response to Ang1-7 in female ovariectomized estradiol treated rats was attenuated compared to nonestradiol treated rats (35) by an unknown mechanism.…”

“…The renal vascular response to Ang1-7 also was gender and sex hormone related. Although the MasR has been known as specified receptor for Ang1-7 however, by MasR antagonist (A779) infusion, the RBF response to Ang1-7 may attenuate in female, and such observation was not seen in male (33). Moreover, by inhibition of AngII receptors (AT1R and AT2R) and Ang1-7 receptor (MasR), the RBF response to Ang1-7 infusion increased in male (not in female) (34).…”

Angiotensin-(1–7) Modulates Angiotensin II-Induced Vasoconstriction in Human Mammary Artery

“…As previously referred, ANG-(1-7) exerts important vasodilator effects in various experimental animal vascular territories, mainly in rat, including aorta [33], renal arteries [34], mesenteric arteries [35] and cerebral arteries [36]. Moreover, a clear benefit of this heptapeptide has been observed in animal models of hypertension through modulation of vascular resistance but also due to relevant effects on kidney, heart and autonomic nervous system [37,38].…”