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作 者:罗蕾[1] 刘爱东[1] 刘红[2] 余德芊[1] 高原[3]
机构地区:[1]遵义医学院生理学教研室,遵义563003 [2]川北医学院生理学教研室,南充637000 [3]遵义医学院珠海校区机能学教研室,珠海519041
出 处:《解剖学杂志》2009年第6期781-784,共4页Chinese Journal of Anatomy
基 金:珠海市科技基金资助项目(PC2003010057)
摘 要:目的:探讨大鼠正中视前核(MnPO)的血管紧张素Ⅱ(AngⅡ)对肾近球小管Na^+,K^+-ATPase活性的作用及其途径。方法:SD大鼠MnPO注射AngⅡ,注射后15、45、60、75、105、145min取肾,分离单根近球小管,测定Na^+,K^+-AT—Pase活性;注射后取血测定血清的内源性洋地黄样物质(EDLS)。结果:与MnP0注射人工脑脊液(aCSF)相比,注射AngⅡ后60min,血清EDLS水平达峰值,近球小管Na^+,K^+-ATPase活性降到最低值,注射后105min,近球小管Na^+,K^+-ATPase的活性和血清EDLS水平分别恢复到对照水平。MnPO注射AngⅡ后145min内的EDLS浓度与其近球小管Na^+,K^+-ATPase活性呈显著负相关。结论:AngⅡ作用于MnPO可抑制近球小管的Na^+,K^+-ATPase活性;AngⅡ在MnPO是通过AT1受体介导的;AngⅡ在MnPO通过AT1受体介导,远距离抑制近球小管Na^+,K^+-ATPase活性的途径,可能与EDLS释放增多有关。Objective: To explore the effect and pathway of activation of angiotensin Ⅱ (Ang Ⅱ ) type 1 receptor (AT1 receptor) in median preoptic nucleus on Na^+,K^+-ATPase activity in proximal tubules. Methods: 15, 45, 60, 75, 105 and 145 rain after Ang Ⅱ mieroinjected into median preoptic nucleus (MnPO), the single proximal tubule of rat kidneys was isolated by means of microdessection to detect Na^+,K^+-ATPase activity. The endogenous digitalis-like substance (EDLS) levels in serum were detected by radioimmunoassay (RIA). Results: Serum EDLS was increased and reached peak at 60 min after injection of Ang Ⅱ. There was a negative linear correlation between EDLS and Na^+,K^+-ATPase activity in proximal tubules. Conclusion. These findings suggest that Ang Ⅱ in MnPO inhibits Na^+,K^+-ATPase aqtivity in proximal tubules, which should be attributed to its capability of modulation of EDLS release via AT1 receptor.
关 键 词:正中视前核 血管紧张素Ⅱ 近球小管 Na^+ K^+-ATPase内源性洋地黄样物质 大鼠
分 类 号:R135[医药卫生—劳动卫生] R544.1[医药卫生—公共卫生与预防医学]
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