Levine D Z, Iacovitti M, Buckman S, Burns K D
Department of Medicine, University of Ottawa, Ontario, Canada.
J Clin Invest. 1996 Jan 1;97(1):120-5. doi: 10.1172/JCI118378.
We have reported that overnight fasting stimulates bicarbonate reabsorption (JtCo2) in rat distal tubules. The present in vivo microperfusion studies evaluated the hypothesis that endogenous angiotensin II (AII) mediates this response. Rat late distal (LD) tubules were perfused at 8 nl/min in vivo with a hypotonic solution containing 28 mM bicarbonate. In overnight-fasted rats, LD JtCO2 was significantly higher than in normally fed rats (50 +/- 4 vs. 16 +/- 6 pmol/min.mm, P < 0.05). When overnight-fasted rats were salt-loaded, JtCO2 fell significantly (38 +/- 3 pmol/min.mm, P < 0.05). Conversely, in fed rats ingesting a zero-salt diet, JtCO2 increased three-fold (45 +/- 5 pmol/min.mm, P < 0.05). Enalaprilat infusion (0.25 micrograms/kg body wt, intravenously), in these zero-salt and overnight-fasted rats, reduced LD JtCO2 values to normal. Further, infusion of losartan (5 mg/kg body wt, intravenously), the specific AII AT1 receptor blocker, reduced JtCO2 in overnight-fasted rats by two-thirds (16 +/- 4 pmol/min.mm, P < 0.05). Finally, we perfused 10(-11) M AII intraluminally with and without 10(-6) M losartan: AII increased JtCO2 to 45 +/- 6 pmol/min.mm, equal to the zero-salt flux. This was completely abrogated by simultaneous losartan perfusion. Therefore, these results suggest that AII is an in vivo stimulator of late distal tubule bicarbonate reabsorption.
我们曾报道过夜禁食可刺激大鼠远端肾小管重吸收碳酸氢盐(JtCo2)。目前的体内微灌注研究评估了内源性血管紧张素II(AII)介导此反应的假说。在体内以8 nl/min的速度用含28 mM碳酸氢盐的低渗溶液灌注大鼠远端肾小管后期(LD)。在过夜禁食的大鼠中,LD的JtCO2显著高于正常喂食的大鼠(50±4 vs. 16±6 pmol/min.mm,P<0.05)。当给过夜禁食的大鼠负荷盐分后,JtCO2显著下降(38±3 pmol/min.mm,P<0.05)。相反,在摄入无盐饮食的喂食大鼠中,JtCO2增加了两倍(45±5 pmol/min.mm,P<0.05)。在这些无盐且过夜禁食的大鼠中,静脉注射依那普利拉(0.25微克/千克体重)可使LD的JtCO2值恢复正常。此外,静脉注射特异性AII AT1受体阻滞剂氯沙坦(5毫克/千克体重)可使过夜禁食大鼠的JtCO2降低三分之二(16±4 pmol/min.mm,P<0.05)。最后,我们在有和没有10(-6) M氯沙坦的情况下向管腔内灌注10(-11) M AII:AII可使JtCO2增加至45±6 pmol/min.mm,与无盐通量相等。同时灌注氯沙坦可完全消除此作用。因此,这些结果表明AII是远端肾小管后期碳酸氢盐重吸收的体内刺激物。