Effects Of Vasonatrin Peptide On Proliferation Of Pulmonary Artery Smooth Cell And Gene Expression Of Natriuretic Peptide B Receptors

The abnormal proliferation of pulmonary artery smooth muscle cell(PASMC) is the main mechanism and pathological changes in pulmonary artery hypertension (PAH) . To study the regulation mechanism of PASMC proliferation is very important for the prevention and therapy of PAH. The abnormal proliferation of PASMC is the result of imbalance between the positive and negative regulator. It is known that atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) can inhibit the proliferation of vascular smooth cell, heart fibroblast cell and cardiac myocyte besides their diuresis, natriuresis and vasodilating action. Vasonatrin peptide(VNP), which is man synthesized , is a chimera of CNP and ANP. VNP has the similar diuresis, natriuresis and vasodilating action to ANP and CNP However, whether VNP has effects on cell proliferation is not clear.There are three subtypes in natriuretic peptide receptors (NPR): natriuretic peptide receptor-A (NPR-A). natriuretic peptide receptor-B (NPR-B) and natriuretic peptide receptor-C (NPR-C) . NPR-A and NPR-B are particulate guanylate cyclase (GC) - coupled receptor. After NPs binding to NPR-A or NPR-B. GC activity of NPR is activated, which catalysed GTP to cGMP. The elevated cGMP. as a second message, mediates the NPs' effects. NPR-C, a clearance receptor, is not coupled to GC and mediates the degradation of NPs. NPR are widely but differently distributed in most tissues and can be up- or down- regulated in many pathological process, which indicate that they have different effects on different tissue and take part in the regulation of these pathological process.