Objective To investigate the calcium-sensing receptor ( CaSＲ) and endogenous NO in the mechanism of the formation of high pulmonary blood flow derived pulmonary hypertension in rat． Method 24 SD rats were randomly divided into pulmonary arterial hypertension group( PAH group) or the control group，with the PAH group were carried out with left lung resection surgery． After 30 day＇s feeding，pulmonary artery mean pressure ( PAMP) were measured by right heart catheterization， right ventricular weight / body weight ( right ventricle / body weight，ＲV / BW) and right ventricle / left ventricle + interventricular septum ( right ventricle / left ventricle plus septum，ＲV / LV + S) ratio were calculated，pulmonary vascular structural changes were observed with optical microscope， plasma NO were detected，and the expression of CaSＲ mＲNA in pulmonary artery endothelial cell were detected by real-time quantitative PCＲ in both groups． Ｒesults PAMP，the ＲV / BW and ＲV / ( LV + S to) the ratio in PAH group were significantly higher ( P ＜0． 05) than those in the control group． Under light microscope，endothelial cell in pulmonary small artery proliferated obviously and the medium membrane thickness increased significantly in PAH group compared to those in the control group． Both the expression of CaSＲ mＲNA in pulmonary artery endothelial celland plasma NO were apparently higher in PAH group than those in the control group． ( all P ＜ 0． 05) ． Conclusion The change in the expression of CaSＲ mＲNA in pulmonary artery endothelial cell with high pulmonary blood flow might involve in the formation of pulmonary artery hypertension by changing the generation of NO and damaging mitochondrium．

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