Impaired post-infarction cardiac remodeling in chronic kidney disease is due to excessive renin release

摘要: The complex pathophysiological interactions between heart and kidney diseases are collectively known as cardiorenal syndrome. renin–angiotensin system (RAS) may have a pivotal role in the development of aim this study was to elucidate RAS activity responsible for adverse post-infarction remodeling prognosis mice with renal failure. To establish type IV syndrome model, 5/6 nephrectomy (NTX) performed surgical procedure, followed by induction myocardial ischemia (MI) coronary artery ligation 4 weeks later. NTX MI resulted deteriorated left ventricular activation, which improved an aliskiren that appeared be independent function blood pressure (BP). Moreover, induced renin angiotensinogen double-transgenic (Tg) showed comparable effects plus mice, including advanced enhancement RAS, oxidative stress, monocytes chemoattractant protein (MCP)-1. Aliskiren suppressed these changes MI-induced Tg mice. In vitro study, Nox2 expression elevated stimulation plasma from isolated neonatal cardiomyocytes. However, upregulation negated when we administered aliskiren-treated-NTX or cardiomyocytes AT1-deficient Primary mononuclear cells also MCP-1 Our data suggest disorder results dysfunction deteriorates after through excessive activation. inhibition caused