摘要
目的:探讨大鼠穹窿下器官(SFO)对外周肾小管钠泵的调节作用及机制。方法:在SFO分别微量注射血管紧张素II(AngII),其中氯沙坦(losartan)组先用AngII的1型受体(AT1)拮抗剂losartan预处理后再注射AngII;放免法检测血清中内源性洋地黄样物质(EDLS)的水平和血浆AngII水平;微分离大鼠肾脏单根近球小管,液闪法测定小管管周膜钠泵活性。结果:①SFO注射AngII后,血清中EDLS在15 min开始升高,约60 min达高峰;②肾近球小管钠泵活性在SFO注射AngII后30 min和60 min都显著下降;③用losartan预处理SFO后,再注射AngII,血清EDLS水平升高和小管钠泵活性下降的效应被显著削弱。结论:大鼠SFO注射AngII后,肾近球小管钠泵活性将下降,原因可能与SFO注射AngII后,激动SFO的AT1受体,直接或间接升高血清EDLS水平有关。
Aim:To investigate the effect of micro-injection AngⅡ into the subfomical organ(SFO) on the proximal tubules (PT) Na^+ , K^+-ATPase activity in rats and its mechanism. Methods: SFO in SD rats was administrated respectively with Ang II(20ng), or losartan(5 pg) and Angll(20ng) successively. The levels of serum EDLS and plasm Angll were assessed with radioimmunoassay (RIA). The PT segments were microdissected freehand and their Na^+ , K^+ -ATPase activities were assessed by liquid scintillation counter(LSC). Results: The serum EDLS levels increased significantly compared with aCSF group after SFO administration with AnglI; The Na^+ ,K^+ -ATPase activities in PT segments decreased significantly at 30 min and 60 min after SFO administration with AnglI. There was a negative linear correlation between serum EDLS level and the Na^+ ,K^+ -ATPase activity of PT segments in rats administrated with AnglI(r = -0. 938). Conclusion: Inhibition of the Na^ + , K^ + -ATPase activity in PT as a result of administration of AnglI in SFO is mediated by AT1 receptors. The increase in EDLS release may play an important role in this inhibition.
出处
《中国应用生理学杂志》
CAS
CSCD
北大核心
2008年第2期229-232,共4页
Chinese Journal of Applied Physiology
基金
四川省教育厅科研基金(2006c015)
南充市重点科技项目(N2006-SF003)
关键词
血管紧张素Ⅱ
穹窿下器
近球小管
内源性洋地黄样物质
钠泵
大鼠
subfornical organ
angiotensin II
proximal tubule
Na^+ , K^+ -ATPase
endogenous digitalis-like substance
rat