Role of peritubular capillary forces in the renal action of carbonic anhydrase inhibitor.
Role of peritubular capillary forces in the renal action of carbonic anhydrase inhibitor.
复制标题
肾小管周围毛细血管力在碳酸酐酶抑制剂肾作用中的作用。
DOI：
10.1038/ki.1986.262
复制
发表时间：
1986
影响因子：
19.6
通讯作者：
Kon,V
中科院分区：
文献类型：
--
作者：
Ichikawa,I;Kon,V
肾小管周围毛细血管力在碳酸酐酶抑制剂肾脏作用中的作用。在Munich-Wistar大鼠中进行微穿刺研究，以评估碳酸酐酶抑制剂抑制近端液体重吸收期间肾浅皮质中的小管周围毛细血管Starling力。给药苯甲酰胺（2 mg/kg/hr，静脉内，第1组（N = 7只大鼠）不仅使近端液体重吸收的绝对速率（APR，从26.7 ± 4.0 nl/min降至17.7 ± 3.6，P < 0.001）降低，而且使肾小管周围跨毛细血管液压差（从10.0 ± 0.5 mm Hg增至15.2 ± 0.5，P < 0.001）增加。在一个单独的7只大鼠组（第2组）中，这些参数在未接受苯甲酰胺治疗的情况下未发生显著变化。在第1组大鼠中，尝试通过输注高渗高红细胞压积血液来抵消苯甲酰胺诱导的小管周围毛细血管净重吸收力的降低。在这种治疗后，当继续给予苯甲酰胺时，APR值恢复到与苯甲酰胺给药前测量的值几乎相同的水平（25.6 ± 4.8 nl/min），与小管周围跨毛细血管压差升高相关。以与第1组相同的方式给药的单独一组6只大鼠显示出在血液输注后碳酸酐酶活性持续抑制，如低水平的全肾碳酸氢盐重吸收率所示。基于第1组中Starling力的测量值计算管周毛细血管重吸收系数，并且在整个研究期间不受影响。单独持续苯甲酰胺给药而不治疗高血压血液没有显著改变APR（第3组，N = 7只大鼠）。这些结果表明，碳酸酐酶抑制剂的管理引起的小管周围毛细血管水摄取力的抑郁症，并维持这种减少的小管周围摄取力是一个必要的抑制影响的碳酸酐酶抑制剂近端水重吸收要充分表达在体内。
Role of peritubular capillary forces in the renal action of carbonic anhydrase inhibitor. Micropuncture study was performed in Munich–Wistar rats to assess peritubular capillary Starling forces in renal superficial cortex during suppression of proximal fluid reabsorption by carbonic anhydrase inhibitor. Administration of benzolamide (2 mg/kg/hr, i.v., Group 1, N = 7 rats) caused not only reduction in absolute rate of proximal fluid reabsorption (APR, from 26.7 ± 4.0 nl/min to 17.7 ± 3.6, P < 0.001), but also an increase in peritubular transcapillary hydraulic–pressure difference (from 10.0 ± 0.5 mm Hg to 15.2 ± 0.5, P < 0.001). In a separate group of seven rats (Group 2), these parameters did not change significantly without benzolamide treatment. In Group 1 rats, an attempt was made to nullify the benzolamide–induced reduction in the peritubular capillary net reabsorptive forces by infusing hyperoncotic high–hematocrit blood. Following this treatment, while benzolamide administration was continued, values for APR returned to levels (25.6 ± 4.8 nl/min) nearly identical to those measured prior to benzolamide administration, in association with a rise in peritubular transcapillary oncotic pressure difference. A separate group of six rats treated in a fashion identical to that of Group 1 showed continued suppression of carbonic anhydrase activity following blood infusion as indicated by low levels of whole kidney bicarbonate reabsorption rate. Peritubular capillary reabsorption coefficient was calculated based on the measured values for Starling forces in Group 1 and were unaffected throughout the study. Continued benzolamide administration alone without the treatment of hyperoncotic blood did not change APR significantly (Group 3, N = 7 rats). These results indicate that administration of carbonic anhydrase inhibitor causes a depression of peritubular capillary water uptake forces, and the maintenance of this reduced peritubular uptake forces is a requirement for the suppressive influence of carbonic anhydrase inhibitor on proximal water reabsorption to be fully expressed in vivo.