Altered regional blood flow distribution in Mas-deficient mice

Abstract

These results suggest that the Ang-(1-7)/Mas axis plays an important role in regional and systemic hemodynamic adjustments in mice.

Mas and Its Related G Protein–Coupled Receptors, Mrgprs

“…Accordingly, cardiomyocytes from Mas-KO mice presented a smaller peak Ca 2+ transient and slower Ca 2+ uptakes due to a decreased expression of SERCA2 (Gomes et al, 2012). These changes were turned into a decreased heart function in Mas-KO mice (Santos et al, 2006;Botelho-Santos et al, 2012;Gava et al, 2012). The changes in the calcium handling proteins were paralleled by changes in the NO production machinery (Dias-Peixoto et al, 2008).…”

“…It has been reported that Mas-deficient mice present an important increase in the vascular resistance in many territories, such as kidney, lung, adrenal gland, mesentery, spleen, and brown fat tissue (Botelho-Santos et al, 2012). A parallel increase in total peripheral resistance and a decreased cardiac index was also observed.…”

International Union of Basic and Clinical Pharmacology. XCIX. Angiotensin Receptors: Interpreters of Pathophysiological Angiotensinergic Stimuli

“…In humans and other species, the endothelial layer of blood vessels produce Ang(1-7) (Santos and Baracho, 1992) and the presence of MAS in endothelial cells and VSMC is conserved, suggesting localized functional interaction da Costa Goncalves et al, 2007;Sampaio et al, 2007b;Xu et al, 2008). Mas knockout increases the vascular resistance in mice in various organs (Botelho-Santos et al, 2012). In the transgenic rats, with increased circulating Ang (1)(2)(3)(4)(5)(6)(7), an Ang(1-7)-dependent vasodilatory tone in blood vessels is suggested.…”

“…In addition the Mas knockout, mice are also reported to have changes in hemostasis (Fraga-Silva et al, 2008) and penile fibrosis (da Costa Goncalves et al, 2007). A common mechanism behind the Mas knockout mice, exhibiting altered heart rate and blood pressure, increased vascular resistance, and decrease blood flow, is thought to be endothelial dysfunction due to imbalances in nitric oxide (NO) and reactive oxygen species (Castro et al, 2005;da Costa Goncalves et al, 2007;Peiro et al, 2007;Rabelo et al, 2008;Xu et al, 2008;Raku san et al, 2010;Botelho-Santos et al, 2012).…”

“…However, an increased uptake and SERCA2 expression in transgenic rats overexpressing Ang(1-7) was reported by Gomes et al (2012). Mas knockout alters expression of calcium handling proteins and decreased contractility of heart in mice Botelho-Santos et al, 2012;Gava et al, 2012;Gomes et al, 2012). The cardiomyocytes in Mas knockout mice increase caveolin 3 expression and decrease HSP90, which reduces eNOS activity (Wu, 2002;Takahashi and Mendelsohn, 2003;Dias-Peixoto et al, 2008).…”