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Cular inflammation (Brecht et al., 2011). 4. Heart. Relaxin acts directly on the heart. The presence of RXFP1 in the heart was first suggested by the demonstration of high-affinity binding sites forHalls et al.relaxin in rat atria (Osheroff et al., 1992; Osheroff and Ho, 1993; Tan et al., 1999). Subsequently, relaxin was shown to be a powerful inotropic and chronotropic agent (Kakouris et al., 19
Mbrane model (McDonald et al., 2003) and in spontaneously hypertensive rats (Lekgabe et al., 2005). In cardiac fibroblasts, relaxin reduces collagen type I and III expression and increases MMPs (Samuel et al., 2004a). In cardiac fibrosis after chronic stimulation of b-adrenoceptors by isoprenaline (Zhang et al., 2005) or by cardiac-specific transgenic overexpression of b2-adrenoceptors (Bathgate
Ributed to relaxin (Heeg et al., 2005; Mookerjee et al., 2009; Chow et al., 2012), including inhibition of the TGF-b1/pSmad2 axis and reduced TGF-b1 nduced collagen deposition. Because AT2Rs are expressed at low levels in tissues (Matsubara, 1998; Carey, 2005; Jones et al., 2008) and fibroblasts under physiologically quiescent states but are dramatically increased in number and activity under pat
S NOS of its substrate L-arginine; antagonizes the increased ET-1 expression that promotes vasoconstriction and inflammation; upregulates SOD-1 expression to combat oxidative/nitrosative stress; and finally, causes partial reversal of dephosphorylation of eNOS, which impairs NO generation. Others have confirmed the SOD-1 finding and also reported elevated SOD-2 expression (Collino et al., 2013).

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