2837

UTS2R

GPR14|UR-2-R|UTR|UTR2;urotensin 2 receptor;UTS2R;urotensin 2 receptor

G protein-coupled receptor 14|G-protein coupled receptor 14|UR-II-R|urotensin II receptor|urotensin-2 receptor

17q25.3

protein-coding

Count: Uts2r; 57305

AIM: To investigate the dynamic changes and functions of urotensin II (U lI) receptor (UT) in pulmonary arteries of rats chronically exposed to hypoxia-hypercapnia. METHODS: In rats with hypoxia-hypercapnia at 1, 2 and 4 weeks U II receptor binding of pulmonary arteries sarcolemma was determined by radioligand assay. U II mRNA and UTmRNA in various grades of pulmonary arterioles were measured by in situ hybridization. RESULTS: (1) Mean pulmonary pressure (mPAP) and weight ratio of right ventricle to left ventricle and septum (RV/LV + S) of 1-week group were higher than those of normal control (NC) group by 26.2% and 21.6% (P < 0.01), respectively, and 2-week group higher than 1-week group by 22.5% and 14.1% (respectively, P < 0.01). However, no significant changes were found between 4-week and 2-week group. (2) U Il receptor (Bmax) of 1-week group was higher than NC group by 38.8%, 2-week group higher than 1-week group by 23.2%, and 4-week group increased 7.3% compared with 2-week group (respectively, P < 0.01). The UT changes were time-dependent, while the affinity to U II (Kd) was no different among each group. (3) UII mRNA in each grade of pulmonary arterioles of 2-week group and 4-week group were higher than NC group (respectively, P < 0.01), and those of 2-week group were higher than 1-week group by 5.9% (P > 0.05), 16.4% and 9.1% (respectively, P < 0.01), while no differences existed between 2-week group and 4-week group. (4) UT mRNA in each grade of pulmonary arterioles of all hypoxia-hypercapnia groups was higher than NC group (respectively, P < 0.01), and those of two abaxial grade vessels in 1-week group were the highest. No differences existed between 2-week group and 4-week group. (5) The pulmonary vessels remodeling were time-dependently aggravated by hypoxia-hypercapnia. CONCLUSION: The dynamic changes of UT in pulmonary arterioles might have important contribution to the development of pulmonary hypertension and pulmonary arteriole remodeling induced by chronic hypoxia-hypercapnia in rats.

AIM: To observe the expression of Urotensin II (U II) and its receptor (UT) on right ventricle in rats with chronic pulmonary hypertension induced by hypoxia and hypercapnia. METHODS: Twenty male SD rats were randomly divided into normal control group (NC) and hypoxia-hypercapnia 4-week group(HH). Mean pulmonary arterial pressure(MPAP) and the weight ratio of right ventricle (RV) to left ventricle plus septum (LV+ S) were calculated separately. U II in plasma was measured using radioimmunoassay. The expression of U II was observed in right ventricle myocytes and right ventricle arteries by immunohistochemistry. The expression of U II mRNA and UT mRNA were observed in right ventricle myocytes and right ventricle arteries by in situ hybridization. RESULTS: (1) The MPAP and RV/LV + S of HH group were higher respectively than those of NC group (P < 0.01, respectively). (2) The plasma U II content of HH group did not increased obviously than that of NC group. (3) The expression score of U II, U II mRNA, UT mRNA by right ventricle myocytes in HH group were higher significantly than those of NC group (P < 0.01 respectively). (4) The average value of integral light density (LD) of U II, U II mRNA, UT mRNA by right cardial arteries in HH group were higher significantly than those of NC group (P < 0.01, respectively). CONCLUSION: The expression of U II in right ventricle arteries and right ventricle myocytes increase significantly during the formation of pulmonary hypertension and right ventricle hypertrophy in rats chronically exposed to hypoxia-hypercapnia. These changes indicate that U II might be involved in right ventricle remodeling, which promotes proliferation of cardiac muscle cells.