Margaret Mylle

The osmolality was determined of fluid collected by micropuncture from proximal and distal convolutions, loops of Henle, collecting ducts and vasa recta of kidneys of various rodents with and without osmotic diuresis. Proximal tubular fluid was isosmotic; in the presence of antidiuretic hormone, early distal fluid was hypo-osmotic due to the prior reabsorption of sodium chloride, and late distal fluid again isosmotic. The hyperosmotic concentration of the urine is established in the collecting ducts, apparently as a consequence, in part at least, of the hyperosmotic reabsorption of sodium chloride in the loops of Henle. Fluid from the bends of loops of Henle, and from collecting ducts and vasa recta at the same level were equally hyperosmotic, consistent with the hypothesis that the mammalian nephron functions as a countercurrent multiplier system. The vasa recta are believed to play an important role in the concentration of the urine by functioning as countercurrent diffusion exchangers.

Methods are described for direct measurement of the hydrostatic pressure in the surface tubules and capillaries of the rat kidney. In fifty-six anesthetized rats intratubular pressure averaged 13.5 ± 2.4 mm Hg. Subsequent microdissection showed that all of the 112 puncture sites so localized were in the first two-thirds of the proximal convoluted tubule. Under all conditions studied, intratubular pressure and the pressure in the peritubular capillaries were approximately the same. Intravenous injection of hypertonic dextrose solution generally produced a brief rise in intratubular and peritubular capillary pressures, which returned to their preinjection levels while the diuresis so produced continued, although at less than the maximal rate. Obstruction of the ureter of kidneys undergoing diuresis resulted in a prompt rise in intratubular pressure, which agreed closely with the simultaneously determined ureteral pressure. Elevation of the ureteral pressure with a pressure bottle had no effect on intratubular or peritubular capillary pressures until it exceeded the pre-existing intratubular and peritubular capillary pressures, and then all rose together up to a maximum intratubular pressure above which elevation of ureteral pressure resulted in no further rise in intratubular or peritubular capillary pressure. Elevation of applied ureteral pressure in kidneys with collapsed tubules and in dead animals did not increase the intratubular pressure, demonstrating that the rise in intratubular pressure produced in this manner in functioning kidneys was not simply a direct back transmission of pressure. Elevation of renal venous pressure by compression of the renal vein also had no effect on intratubular and peritubular capillary pressures until their pre-existing values were exceeded, and then all three pressures rose together.

Anesthetized, nondiuretic rats and hamsters were infused with C 14 -labeled inulin-carboxylic acid or urea, and fluid was subsequently collected by micropuncture from surface tubules in the rats and from loops of Henle and collecting ducts in the hamsters. Osmolality and radioactivity of tubular fluid, ureteral urine, and plasma were determined. There was net loss of both water and solute from all segments of the nephron. In the loop of Henle, water loss occurred primarily from the descending limb and solute loss from the ascending limb. Urea was reabsorbed from the proximal and distal convolutions and collecting ducts but was added to the tubular fluid in the descending limb of the loop of Henle. These results lend support to the countercurrent theory of urine concentration and indicate that the osmotic gradient in the medulla is established by active transport of solute out of the ascending limb of the loop of Henle. The results are compatible with passive movement of water and urea, but the possibility of active transport of urea is not excluded.

Anesthetized rats and hamsters were given Ca 45 intravenously, and fluid was subsequently collected by micropuncture from glomeruli and surface tubules in the rats, and from loops of Henle in the hamsters. In nondiuretic animals, fluid:plasma calcium ratios averaged 0.71 in the glomerulus; 0.76 in the proximal tubule; 2.0 in the loop of Henle; 0.47 in the distal convolution; and 0.9 in ureteral urine. In mannitol diuresis, the calcium ratio of glomerular fluid was unchanged, but ratios as low as 0.21 were noted in the proximal tubule. In this circumstance, the average proximal ratio was 0.61, and the distal ratio 0.07. These results indicate active transport of calcium out of all major parts of the nephron, with the bulk of calcium reabsorption occurring in the convoluted portion of the proximal tubule. Furthermore, the pattern of tubular reabsorption of calcium is similar to that of sodium, suggesting that the two are related.

Fluid was collected by micropuncture from individual renal tubules of anesthetized rats and its pH determined with the quinhydrone microelectrode. The single glomerular sample and early proximal fluid were isohydric with arterial blood, but later proximal fluid usually showed progressive acidification. The maximum proximal fall in pH was 0.43 u in nondiuretic rats, 0.56 u during profuse glucose or mannitol diuresis, and 0.78 u in rats previously loaded with ammonium chloride and undergoing glucose diuresis. Fluid from the early distal convolution was usually acidified relative to arterial blood but was not significantly different from late proximal fluid. Progressive acidification probably also occurred in the distal convolution. The pH decreased further in the collecting ducts, much more so in the nondiuretic state than during diuresis. The quantitative importance of proximal reabsorption of HCO 3 – and, by inference, H + secretion is emphasized. It is suggested that the pH of tubular fluid may increase in the thin descending limb of the loop of Henle, especially in a kidney elaborating a concentrated urine, because of increased concentration of HCO 3 – .