摘要
浓度为1.0～18.0nmol/L的内皮素可引起大鼠主动脉产生浓度依赖性收缩,其EC_(50)为3.75±0.75nmol/L。正常对照组中平滑肌细胞S+G_2M期细胞的比例基本稳定在26.3～29.6％的范围内;浓度为10.0和100.0pmol/L的内皮素可使S+G_2M期细胞呈浓度依赖性(P<0.01)和时间依赖性(P<0.01)增加。10.0pmol/L的内皮素作用30min后ATP含量经短暂升高后维持在低水平。结果表明内皮素具有缩血管作用及促进平滑肌细胞增生的作用,上述作用可能在高血压发病机制中有一定的意义。
Endothelin is one of the most potent vasoconstrictors known to date. The roles, as well as the mechanisms that endothelin plays in hypertensive diseases have absorbed much attention since its discovery. Our work studied the roles of endothelin on the contraction of rat aorta, in vitro, the proliferation and ATP content of cultured vascular smooth muscle cells from rat aorta.
Endothelin could induce a dose-dependent contractile action to rat aorta from the concentration of 1.0 to 18.0 nmol/L and the EC_(50) value was 3.75±0.75nmol/L. Under normal condition, the percentages of proliferative cells (S+G_2M phase) of cultured vascular smooth muscle cells were among 26.3-29.6%; endothelin had a dose-dependent (P<0.01) and a time-dependent (P<0.01) proliferative action to cultured vascular smooth cells. 24 hrs after endothelin action, the percentages of proliferative cells separately increased as high as to 40.7% and 45.6% at concentrations of 10.0 and 100.0 pmol/L. 10.0 pmol/L endothelin could induced a temporary increasing (139.05 ±1.11%, P<0.01) of ATP contents in cultured vascular smooth muscle cells compared with the control group at 10 min after endothelin action, but 20 min after endothelin action, the ATP level drop sharply to 65.25±5.09% (P<0.01) and at 30 min, the ATP level recovered a little (71.13±4.04%; P<0.01) but still lower than normal standard.
Our results showed that (1) endothelin can induce dose-dependent vasoconstriction of rat aorta; (2) endothelin also has a proliferativer ole to cultured vascular smooth muscle cells; (3) the change of ATP contents implies that endothelin-induced responses of vascular smooth muscle cells are energy-consuming course.
出处
《军医进修学院学报》
CAS
1992年第4期317-320,共4页
Academic Journal of Pla Postgraduate Medical School
