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Ere the first biologic effects to be recorded (Hisaw, 1926), and a number of studies have examined this property as a possible treatment of the connective tissue disease scleroderma. Relaxin was safe and well tolerated in clinical trials and effective in some patients in a phase II trial (Seibold et al., 2000) but failed to show clinical efficacy in a larger scale phase III trial (Erikson andUnem
Ere the first biologic effects to be recorded (Hisaw, 1926), and a number of studies have examined this property as a possible treatment of the connective tissue disease scleroderma. Relaxin was safe and well tolerated in clinical trials and effective in some patients in a phase II trial (Seibold et al., 2000) but failed to show clinical efficacy in a larger scale phase III trial (Erikson andUnem
St SU5416 blocks the vasorelaxant effects of relaxin (McGuane et al., 2011a), the specificity of SU5416 has been questioned (Arora and Scholar, 2005; Loges et al., 2006), and in rat renal arteries, SU5416 potentiates the acute vasodilator effects of relaxin (McGuane et al., 2011b). Furthermore, although VEGF-neutralizing antibodies block the effects of relaxin, this can also be mimicked by placen
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).
Onation, and therefore relaxin deficient, exhibited a decreased glomerular filtration rate compared with that observed in normal pregnancies (Smith et al., 2006b). In a small study in human volunteers (Smith et al., 2006a), relaxin administered for 5 hours increased renal plasma flow by ;75 and fractional sodium excretion by ;25 but did not affect glomerular filtration rate (Smith et al., 2006a
Nd the positive inotropic effects occur in left atria (Kakouris et al., 1992; Ward et al., 1992; Wade et al., 1994; Tan et al., 1998; Mathieu et al., 2001). Chronotropic effects of relaxin are accompanied by the secretion of atrial natriuretic peptide in isolated perfused rat hearts (Toth et al., 1996). In rabbit sinoatrial node cells, relaxin increases the rate of spontaneous action potentials a
Nd the positive inotropic effects occur in left atria (Kakouris et al., 1992; Ward et al., 1992; Wade et al., 1994; Tan et al., 1998; Mathieu et al., 2001). Chronotropic effects of relaxin are accompanied by the secretion of atrial natriuretic peptide in isolated perfused rat hearts (Toth et al., 1996). In rabbit sinoatrial node cells, relaxin increases the rate of spontaneous action potentials a
Et al., 2002; Zhang et al., 2005). After the demonstration of protective actions in the cardiovascular system, relaxin was tested in human heart failure. A hemodynamic pilot study in patients with stable chronic heart failure (Dschietzig et al., 2009c) demonstrated that a 24-hour intravenous infusion of recombinant human relaxin markedly elevated cardiac index without affecting heart rate and dec
N renal plasma flow and glomerular filtration rate (Smith et al., 2006a), or the effect may take longer to develop via alteration of the filtration coefficient. For example, during chronic relaxin infusion in the scleroderma trials, the estimated glomerular filtration rate rose significantly in the treated group (Seibold et al., 2000; Khanna et al., 2009). However, the vasodilator effects of rela
N renal plasma flow and glomerular filtration rate (Smith et al., 2006a), or the effect may take longer to develop via alteration of the filtration coefficient. For example, during chronic relaxin infusion in the scleroderma trials, the estimated glomerular filtration rate rose significantly in the treated group (Seibold et al., 2000; Khanna et al., 2009). However, the vasodilator effects of rela
Ung (Samuel et al., 2003b), kidney (Samuel et al., 2004b), and heart (Samuel et al., 2004a) by the administration of relaxin. In the lung, treatment with relaxin reduces expression of collagen types I and III, increases levels of MMPs, and reduces fibrosis (Unemori et al., 1996). In kidney-derived fibroblasts, relaxin inhibits profibrotic changes induced by TGF-b by a mechanism involving the NO/g
Usion of the left anterior descending coronary artery, attenuated leukocyte recruitment and oxidative damage and improved contractile recovery (Perna et al., 2005). In a mouse infarction model, relaxin improves postinfarction remodeling by suppressing reactive fibrosis in vital myocardium, without affecting reparative fibrosis (scarring) within the infarcted area (Samuel et al., 2011). This posti
Ly challenging clinical syndrome. 5. Kidney. The pronounced effects of relaxin on renal arteries imply a pivotal role in the regulation of renal function. Indeed, relaxin is the major renal vasodilator responsible for the increases in renal plasma flow and glomerular filtration rate during rat pregnancy (Novak et al., 2001). The increase in renal plasma flow and glomerular filtration rate with re
Effects on geometric remodeling (increases in unstressed wall area and wall-to-lumen area ratio) and compositional remodeling (decrease in collagen-to-total protein ratio) in certain arteries (Chan and Cipolla, 2011; Debrah et al., 2011; Gooi et al., 2013). These properties expedite tissue and organ perfusion in the long term. Compared with arteries, remarkably little is known of the effects of r
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