Expression of Urotensin II and its receptor on right ventricle in rats of pulmonary hypertension.
- Author:
Hong HUANG
1
;
Yong-Sheng GONG
;
Xiao-Fang FAN
;
Liang-Gang HU
;
Jian-Feng LUO
;
Xiao-Mai WU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Heart Ventricles; metabolism; Hypertension, Pulmonary; metabolism; Hypoxia; metabolism; Male; Rats; Rats, Sprague-Dawley; Receptors, G-Protein-Coupled; metabolism; Urotensins; metabolism
- From: Chinese Journal of Applied Physiology 2006;22(1):81-84
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo 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.
METHODSTwenty 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).
CONCLUSIONThe 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.