Quan A, Baum M
Department of Pediatrics, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235-9063, USA.
Am J Physiol. 1998 Jul;275(1):F74-8. doi: 10.1152/ajprenal.1998.275.1.F74.
In the present study, we examined whether the effect of endogenously produced angiotensin II on proximal tubule transport in the male Sprague-Dawley rat is regulated by acute changes in extracellular volume. We measured the magnitude of endogenous angiotensin II-mediated stimulation of transport by sequentially perfusing proximal tubules in vivo, first with an ultrafiltrate-like solution, then by reperfusion of the same tubule with an ultrafiltrate-like solution containing 10(-8) M losartan (angiotensin II receptor antagonist). During volume contraction, 10(-8) M losartan decreased volume reabsorption from 4.20 +/- 0.50 to 1.70 +/- 0.30 nl . mm-1 . min-1 (P < 0.05), a decrease of 58.0 +/- 7.0%. In contrast, after acute volume expansion, 10(-8) M losartan decreased volume reabsorption from 1.84 +/- 0.20 to 1.31 +/- 0.20 nl . mm-1 . min-1 (P < 0.05), a decrease of 29.6 +/- 9.0%. In hydropenic rats, addition of exogenous luminal angiotensin II had no effect on transport. However, in volume-expanded rats, addition of 10(-8) M angiotensin II increased volume reabsorption from 2.10 +/- 0.34 to 4. 38 +/- 0.59 nl . mm-1 . min-1 (P < 0.005). These data are consistent with endogenously produced angiotensin II augmenting proximal tubule transport to a greater degree during volume contraction than after volume expansion.
在本研究中，我们检测了内源性生成的血管紧张素II对雄性Sprague-Dawley大鼠近端小管转运的影响是否受细胞外液量急性变化的调节。我们通过在体内依次灌注近端小管来测量内源性血管紧张素II介导的转运刺激强度，首先用类似超滤液的溶液灌注，然后用含有10(-8) M氯沙坦（血管紧张素II受体拮抗剂）的类似超滤液的溶液对同一小管进行再灌注。在容量收缩期间，10(-8) M氯沙坦使容量重吸收从4.20±0.50降至1.70±0.30 nl·mm-1·min-1（P<0.05），降低了58.0±7.0%。相反，在急性容量扩张后，10(-8) M氯沙坦使容量重吸收从1.84±0.20降至1.31±0.20 nl·mm-1·min-1（P<0.05），降低了29.6±9.0%。在缺水大鼠中，添加外源性管腔血管紧张素II对转运无影响。然而，在容量扩张的大鼠中，添加10(-8) M血管紧张素II使容量重吸收从2.10±0.34增加至4.38±0.59 nl·mm-1·min-1（P<0.005）。这些数据表明，内源性生成的血管紧张素II在容量收缩期间比容量扩张后能更大程度地增强近端小管的转运。
