大鼠脑室内注射ANGⅡ和ANGⅡ抗体对尿钠排出和肾皮质Na^+·K^+-ATPase的影响

EFFECT OF INTRACEREBROVENTRICULAR INJECTIONS OF ANG Ⅱ AND ANG Ⅱ ANTIBODY ON RENAL SODIUM EXCRETION AND Na^+·k^+-ATPase IN RAT

在麻醉大鼠的侧脑室注射16pg血管紧张素Ⅱ(ANGⅡ),15min内出现尿钠增多的反应并持续90min,平均动脉血压保持稳定。肾皮质Na^+·K^+-ATPase活性(1.51±0.26μmolPi/mg Pro·h)显著低于侧脑室注射人工脑脊液的对照值(2.66±0.28μmol Pi/mg Pro·h,P<0.01),而侧脑室注射ANGⅡ抗体后5min内则出现尿钠减少的反应并持续135min。肾皮质Na^+·K^+-ATPase活性(3.61±0.34μmol Pi/mg Pro·h)显著高于对照值(P<0.05)。股静脉和脊髓蛛网膜下腔分别注射16pg ANGⅡ,均未出现尿钠增多的反应。结果表明,脑内的内源性ANGⅡ具有引起尿钠增多的作用;并提示这种作用可能与肾脏Na^+·K^+-ATPase活性的抑制有关。

In anesthetized rats, it was observed that intracerebroventricular (I. C. V.)microinjection of angiotensin Ⅱ(ANG Ⅱ) in a dose of 16 pg evoked a significantincrease in renal sodium excretion which began within 15 min and lasted for 90min. The activity of Na^+·K^+-ATPase in renal cortex after I. C. V. microinjectionof ANG Ⅱ(1.51±0.26μmol Pi/mg Pro·h) was inhibited as compared with thatof the control injecting of artificial cerebrospinal fluid (2.66±0.28 μmol Pi/mgPro·h, P<0.01). There was no change in mean arterial pressure. Within 15min after I. C. V. administration of ANG Ⅱ antibody, however, and antinatri-uretic period of 135 min and a higher activity of Na^+·K^+-ATPase in renal cortex(3.61±0.34 μmol Pi/mg Pro·h, P<0.05 compared with control) were observed.There was no natriuresis in the animals microinjected with ANG Ⅱ either intofemoral vein or into spinal subarachnoid space. The result of the presentinvestigation suggests that brain endogenous ANG Ⅱ may possess some natriureticactivity possibly through inhibiting renal Na^+·K^+-ATPase activity.