CAJ | 학술논문

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~+-ATPase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MnPO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.
목적:탐토대서정중시전핵(MnPO)적혈관긴장소Ⅱ(AngⅡ)대신근구소관Na~+, K~+-ATPase활성적작용급기도경.방법:SD대서MnPO주사AngⅡ,주사후15、 45、 60、 75、 105、 145min취신,분리단근근구소관,측정Na~+, K~+-ATPase활성;주사후취혈측정혈청적내원성양지황양물질(EDLS).결과:여MnPO주사인공뇌척액(aCSF)상비,주사AngⅡ후60min,혈청EDLS수평체봉치,근구소관Na~+, K~+-ATPase활성강도최저치,주사후105min,근구소관Na~+, K~+-ATPase적활성화혈청EDLS수평분별회복도대조수평.MnPO주사AngⅡ후145min내적EDLS농도여기근구소관Na~+, K~+-ATPase활성정현저부상관.결론:AngⅡ작용우MnPO가억제근구소관적Na~+, K~+-ATPase활성;AngⅡ재MnPO시통과AT1수체개도적;AngⅡ재MnPO통과AT1수체개도,원거리억제근구소관Na~+, K~+-ATPase활성적도경,가능여EDLS석방증다유관.
Objective: To explore the effect and pathway of activation of angiotensin Ⅱ (AngⅡ) type 1 receptor (AT1 receptor) in median preoptic nucleus on Na~+, K~+-ATPase activity in proximal tubules.Methods: 15, 45, 60, 75, 105 and 145min after AngⅡ microinjected 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 60min after injection of AngⅡ. There was a negative linear correlation between EDLS and Na~+, K~+-ATPase activity in proximal tubules. Conclusion: These findings suggest that AngⅡ in MnPO inhibits Na~+, K~+-ATPase activity in proximal tubules, which should be attributed to its capability of modulation of EDLS release via AT1 receptor.