AIM: To investigate the changes of vascular endothelial growth factor (VEGF) in the pulmonary circulation of rats with different hypoxia and hypercapnia duration. METHODS: Forty SD rats were randomly divided into normol control group (N), exposed to hypoxia hypercapnia for 2 weeks group (T), for 4 weeks group (F), for 8 weeks group (E). The levels of VEGF were measured and the ultrastructure of pulmonary arterioles was observed by electron microscopy. RESULTS: Mean pulmonary arterial pressure (mPAP), weight ratio of RV to LV+S, the levels of VEGF in serum and lung tissue, the expression of VEGF and VEGF mRNA in group T, F, E were significantly higher than that in group N. With the prolong duration, base of endothelial cell was narrowed, proliferation of smooth muscle cells and collagenous fibers of pulmonary arterioles in rats were increased gradually. CONCLUSIONS: Hypoxia and hypercapnia increase the expression of VEGF mRNA and synthesis of VEGF. VEGF may play an important role in the pathogenesis of hypoxia pulmonary hypertension and reconstruction of pulmonary artery.

AIM:To investigate rat Urotensin-II(ra t U-II)-induced vasoconstriction of rat main pulmonary arteries and the role of mitogen-activated protein kinase(MAPK). METHODS: The main pulmon ary artery was dissected from the male Sprague -Dawley rats and artery ring width was 3-4 mm. Concentration-response curves wer e gene rated to rat U-II(0 03 nmol/L-30 nmol/L).Inhibitor of MAPK,PD 98059(0 1 ?mol/ L -10 ?mol/L) were added into the medium after rat U-II(30 nmol/L)induced vasoc onstriction had reached plateau to construct the relaxant concentration-respons e curves and their EC 50 and E max . RESULTS: Rat U-II was a potent vasoconstrictor of isolated rat main pulmonary arteries [EC 50 =7 95?0 4 0, E max =(14 28?6 34)% of the response to 60 mmol/L KCl]; PD 98059 caused c oncentration-dependent relaxations of rat U-II precontracted arteries [EC 50 =5 91?0 45, E max =(81 39?13 65)%]. CONCLUSION: Rat U- II was a potent vasoconstrictor of rat main pulmonary arteries and this response was med iated through MAPK.