Effects Of Ang-(1-7) On Proliferation And Collagen Synthesis Of Rat Cardiac Fibroblasts Induced By Vasopressin And Its Possible Signal Transduction Mechanism

Background Left ventricular hypertrophy is regarded as an independent risk factor for the morbidity of cardiovascular events, so the prevention and regression of left ventricular hypertrophy has been the chief goal of the treatment to essential hypertension. Myocardial fibrosis, which is mainly caused by the abnormal proliferation and collagen synthesis of cardiac fibroblasts(CFs) is one of the pathological bases of left ventricular hypertrophy. Large amount of studies demonstrate that the activation of neuroendocrine factors in tissues and blood circulation is the most impotant reason and motivation in the development of proliferation and collagen synthesis of CFs and Renin-angiotensin system(RAS) plays a significant role in it. Angiotensin-(1-7)[Ang-(1-7)] as a novel peptide of RAS also plays an important role in hypertension and it's associated disease. It has been found so far that the physiological function of Ang-(1-7) includes vasodilation and antihypertensive actions, diuresis and natriuresis. It has also been observed recently that Ang-(1-7) could inhibit proliferation of endotheliocytes and vascular smoothe muscle cells. Thus Ang-(1-7) may participate in the prevention...