Brenner B M, Troy J L
J Clin Invest. 1971 Feb;50(2):336-49. doi: 10.1172/JCI106501.
We tested the relationship between postglomerular microvascular protein concentration and rates of sodium and water transfer by rat proximal tubules. Using recently described microperfusion techniques, efferent arterioles and branch peritubular capillaries of normal hydropenic rats were perfused with colloid-free Ringer's solution, and isoncotic (9.0-10.0 g/100 ml) and hyperoncotic (15 g/100 ml) albumin-Ringer's solutions. Reabsorption in adjacent proximal tubules was studied using free-flow techniques, with initial collections obtained during normal blood perfusion, recollections during experimental microperfusion, and in some tubules, repeat recollections after microperfusion and spontaneous resumption of blood perfusion. Colloid-free perfusion resulted in a uniform inhibition of proximal reabsorption (absolute and fractional). Despite identical techniques, substitution of isoncotic and hyperoncotic perfusates resulted, on average, in unchanged and increased rates of reabsorption, respectively. These findings of direct linear changes in reabsorption in response to changes in postglomerular protein concentrations usually occurred in the absence of significant changes in filtered load, and were nearly always found to be reversible within minutes of cessation of experimental perfusion. Given this evidence of a causal relationship between postglomerular oncotic pressure and proximal reabsorption, we undertook to determine whether this relationship is responsible for the parallel adjustments in proximal reabsorption that follow changes in GFR (glomerulotubular balance). Using a separate group of hydropenic rats, proximal reabsorption was studied, initially during partial aortic constriction (during which renal perfusion pressure, single nephron GFR, absolute proximal reabsorption, and calculated filtration fraction all were reduced below levels prior to constriction), and again while adjacent efferent arteriolar and peritubular capillary protein concentrations, but not GFR, were restored to normal (preconstriction) levels by microperfusion with 9-10 g/100 ml albumin-Ringer's solution. During this dissociation of GFR and postglomerular protein concentration, absolute and fractional proximal reabsorption nearly always increased in parallel with the changes in the latter, thereby demonstrating that glomerulotubular balance is mediated, at least in part, by changes in postglomerular oncotic pressure brought about by changes in filtration fraction.
我们测试了大鼠近端肾小管球后微血管蛋白浓度与钠和水转运速率之间的关系。采用最近描述的微灌注技术,用无胶体的林格氏液、等渗(9.0 - 10.0 g/100 ml)和高渗(15 g/100 ml)白蛋白 - 林格氏液灌注正常缺水大鼠的出球小动脉和肾小管周围毛细血管分支。使用自由流动技术研究相邻近端肾小管的重吸收,在正常血液灌注期间进行初始收集,在实验微灌注期间进行再次收集,并且在一些肾小管中,在微灌注后及血液灌注自发恢复后进行重复收集。无胶体灌注导致近端重吸收(绝对重吸收和分数重吸收)均匀受到抑制。尽管技术相同,但分别用等渗和高渗灌注液替代后,平均而言,重吸收率分别保持不变和增加。这些关于重吸收随球后蛋白浓度变化呈直接线性变化的发现,通常在滤过负荷无显著变化的情况下出现,并且几乎总是发现在实验灌注停止后几分钟内是可逆的。鉴于有证据表明球后胶体渗透压与近端重吸收之间存在因果关系,我们着手确定这种关系是否是肾小球滤过率(GFR)变化后近端重吸收平行调节(球管平衡)的原因。使用另一组缺水大鼠,研究近端重吸收,最初在部分主动脉缩窄期间(在此期间肾灌注压、单个肾单位GFR、绝对近端重吸收和计算的滤过分数均降至缩窄前水平以下),然后再次在相邻出球小动脉和肾小管周围毛细血管蛋白浓度恢复到正常(缩窄前)水平(但GFR未恢复)时进行研究,此时通过用9 - 10 g/100 ml白蛋白 - 林格氏液进行微灌注来实现。在GFR与球后蛋白浓度分离的过程中,绝对和分数近端重吸收几乎总是与后者的变化平行增加,从而表明球管平衡至少部分是由滤过分数变化引起的球后胶体渗透压变化介导的。