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机构地区:[1]遵义医学院生理学教研室,贵州遵义563003
出 处:《遵义医学院学报》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)
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.
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
分 类 号:R331[医药卫生—人体生理学]
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