Franckson J R, Gassée J P, Ooms H A, Dubois R
Curr Probl Clin Biochem. 1976;6:223-37.
The role of renal tubules was explored by two kinds of experiments: (1) inhibition of the tubular reabsorption of insulin by induced polyuria; (2) suppression of insulin filtration by ureter clamping; 1. Anaesthetized dogs maintained in normoglycaemia by glucose compensation were infused with crystalline and 125I-insulins. Polyuria was induced by: (1) saline-bicarbonate infusion; (2) furosemide with saline-bicarbonate infusion to replace urine losses; (3) massive infusion of mannitol. Inulin and paraminohippuric acid were used to estimate the glomerular filtration rate and the renal plasma flow. The permeability of the glomerular wall (pore radius and total area of the pores per unit of path length) was determined by measuring the sieving curve of 131I-polyvinyl-pyrrolidone fractions during basal and treatment periods. Mannitol infusion was able to bring the insulin/inulin clearance ratio up the values of the sieving coefficient of insulin (insulin filtration rate) without modifying the permeability of the glomerular wall; saline infusion displayed a similar effect; furosemide, only a minute one although it induced a more marked polyuria. 2. Clamping of the left ureter was performed on dogs with catheters inserted into the artery, the left renal vein, the pelvis and a renal lymphatic vessel. Almost complete suppression of the glomerular filtration was achieved. It slightly increased the high insulinic concentration of the renal lymph, entailed a 1/3 decrease in the extraction ratio of insulin and reduced by half its renal clearance. In conclusion, the tubules participate to the catabolism of insulin by two different mechanisms: (1) an uptake from the tubular fluid which can be inhibited by diuretics exerting their main action on the proximal tubules; (2) a direct catabolism from the interstitial fluid resulting from the large permeability of the peritubular capillaries to insulin.
(1)通过诱导多尿抑制胰岛素的肾小管重吸收;(2)通过输尿管夹闭抑制胰岛素滤过;1. 对通过葡萄糖补偿维持正常血糖水平的麻醉犬输注结晶胰岛素和125I标记的胰岛素。通过以下方式诱导多尿:(1)输注生理盐水 - 碳酸氢盐;(2)呋塞米联合输注生理盐水 - 碳酸氢盐以补充尿丢失;(3)大量输注甘露醇。使用菊粉和对氨基马尿酸来估计肾小球滤过率和肾血浆流量。通过测量基础期和治疗期131I - 聚乙烯吡咯烷酮组分的筛分曲线来确定肾小球壁的通透性(孔径半径和单位路径长度的孔隙总面积)。输注甘露醇能够使胰岛素/菊粉清除率比值升高至胰岛素筛分系数(胰岛素滤过率)的值,而不改变肾小球壁的通透性;输注生理盐水显示出类似的效果;呋塞米虽然诱导了更显著的多尿,但只有微小的作用。2. 对插入动脉、左肾静脉、肾盂和肾淋巴管导管的犬进行左输尿管夹闭。几乎完全抑制了肾小球滤过。这略微增加了肾淋巴液中高浓度的胰岛素,使胰岛素的提取率降低了1/3,并使其肾清除率降低了一半。总之,肾小管通过两种不同机制参与胰岛素的分解代谢:(1)从肾小管液中摄取,可被主要作用于近端小管的利尿剂抑制;(2)由于肾小管周围毛细血管对胰岛素的高通透性,从间质液中直接进行分解代谢。