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17β-雌二醇抑制雄性大鼠颈动脉窦压力感受器反射
作者姓名:Wang S  Fan ZZ  He RR
作者单位:河北医科大学基础医学研究所生理室,石家庄,050017
摘    要:采用隔离灌流麻醉雄性大鼠颈动脉窦技术 ,观察了 17β 雌二醇 (E2 )对颈动脉窦压力感受器反射的影响。结果如下 :(1)以E2 (10 μmol/L)隔离灌流颈动脉窦区时 ,压力感受器机能曲线向右上方移位 ,曲线最大斜率(peakslope,PS)由 0 49± 0 0 3降至 0 2 5± 0 0 1(P <0 0 1) ,反射性血压下降幅度 (reflexdecrease,RD)由 7 37± 0 42kPa降至 3 49± 0 2 0kPa (P <0 0 0 1) ,阈压 (thresholdpressure ,TP)和饱和压 (saturationpressure ,SP)分别由 9 5 2±0 6 8kPa和 2 4 5 3± 0 48kPa增至 13 3± 0 11kPa (P <0 0 0 1)和 2 7 5 2± 0 2 0kPa (P <0 0 1) ,其中PS、RD、TP和SP呈明显的剂量依赖性 ;(2 )用雌激素受体阻断剂tamoxifen (1、5、10、30 μmol/L)预处理后 ,不能阻断E2 对压力感受器反射的抑制作用 ;(3)预先灌流NO合酶阻断剂 (L NAME ,10 0 μmol/L) ,可完全消除E2 (10 μmol/L)对压力感受器反射的抑制效应。以上结果表明 ,17β 雌二醇可通过非基因组机制抑制大鼠颈动脉窦压力感受器反射 ,其效应系E2 引起血管内皮细胞释放NO所致。

关 键 词:雌激素  压力感受器反射  平均动脉压  血管

17beta -estradiol inhibits carotid sinus baroreflex in male rats
Wang S,Fan ZZ,He RR.17beta -estradiol inhibits carotid sinus baroreflex in male rats[J].Acta Physiologica Sinica,2000,52(6):445-449.
Authors:Wang S  Fan Z Z  He R R
Institution:Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017.
Abstract:By perfusing isolated carotid sinus, the effect of 17beta-estradiol (E(2)) on carotid sinus baroreflex was observed in anesthetized male rats. The results obtained are as follows. (1) By perfusing with E(2) (10 micromol/L), the functional curve of baroreflex was shifted to the right and upward, with a peak slope (PS) decrease from 0.49+/-0.03 to 0.25+/-0.01 (P<0.01) and a reflex decrease in mean arterial pressure (reflex decrease, RD) from 7.37+/-0.42 kPa to 3.49+/-0.20 kPa (P<0.001), while the threshold pressure (TP) and saturation pressure (SP) were significantly increased from 9.52+/-0.68 kPa to 13.3+/-0.11 kPa (P<0.001) and 24.53+/-0.48 kPa to 27.52+/-0.20 kPa (P<0.01) respectively. Among the functional parameters of carotid baroreflex, the changes of RD, PS, TP and SP were dose-dependent. (2) Pretreatment with different doses of tamoxifen (1, 5, 10, 30 micromol/L), an inhibitor of estrogen receptor, did not block the effect of E(2) on carotid baroreflex. (3) Preperfusion with an inhibitor of NO synthase L-NAME (100 micromol/L) could completely abolish the effect of E(2) on carotid baroreflex. It is concluded that the inhibitory effect of E(2)on carotid sinus baroreflex may be mediated by NO release from endothelial cells, but not by a genomic mechanism.
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