摘要
目的大鼠第三脑室前腹侧区(anteroventral part of the third ventricle,AV3V)注射血管紧张素Ⅱ(angio- tensin Ⅱ,AngⅡ)及血管紧张素Ⅱ阻断剂沙拉新(saralasin,sar．)预处理后再注射AngⅡ,测定尿钠排出量、血清内源性洋地黄样因子(endogenous digitalis-like factor,EDLF)浓度和肾皮质Na+,K+-ATP酶活性。结果①大鼠AV3V 注射AngⅡ后尿钠排出量明显升高。②大鼠AV3V注射AngⅡ后血清EDLF浓度明显高于对照组(P<0．05)。③ AV3V注射AngⅡ后,肾皮质Na+,K+-ATP酶活性显著低于对照组(P<0．05)。④大鼠肾皮质Na+,K+-ATP酶活性与血清EDLF浓度呈负相关关系,相关系数-0．932(P<0．05)。结论脑内Ang Ⅱ作用于AV3V的AngⅡ受体,引起尿钠排出增多,这种作用可能与AV3V注射AngⅡ引起EDLF的释放。从而抑制肾皮质Na+,K+-ATP酶的活性有关。
Objective To study the effect of anteroventral part of the third ventricle（AV3V） injection of angiotensin Ⅱ （ Ang Ⅱ ）on endogenous digitalis-like factor（EDLF） release, renal sodium excretion and renal cortical Na^＋, K^＋ -ATPase activity in anesthetized rats. Results AV3V injection Ang Ⅱ induced significant natrjuresis（ P 〈 0.05 ） and inceased the level of EDLF（ P 〈 0.05 ）, decreased renal cortical Na^＋ , K^＋ -ATPase activity （ P 〈 0.05 ） o These effects could be antagonized by AV3V pretreatement of saralasin ,a Ang Ⅱ receptor antagonist. There was a negative linear correlation between serum EDLF level and renal cortical Na^＋, K^＋ -ATPase activity in the rat （ r= - 0.932, P 〈 0.05 ）. Conclusions These result suggest that central Ang Ⅱ may possess natriurctic activity possibly through elevation of serum EDLF levels and inhibition renal cortical Na^＋, K^＋ -ATPase activity.
出处
《合肥医学院学报》
2005年第6期517-520,共4页
Journal of Zunyi Medical University
基金
贵州省卫生厅基金(D-146)
关键词
第三脑室前腹侧区
血管紧张素Ⅱ
内源性洋地黄样因子
尿钠排出
肾皮质Na^+K^+ATP酶
anterovantral part of the third vantricle
angiotensin Ⅱ
endogenous digitalis -like factor
renal sodium excretion
renal cortical Na^＋, K^＋ -ATPase activity.
