Collecting Duct Fluid Research Articles

INTRARENAL DISTRIBUTION OF AMMONIA DURING DIURESIS AND ANTIDIURESIS.

The intrarenal distribution of ammonia was evaluated in the dog during antidiuresis and osmotic (mannitol) diuresis at various levels of urine pH. During antidiuresis, the concentration of ammonia in renal tissue water rose progressively from the cortex to the tip of the papilla. In contrast, the corticomedullary ammonia gradient was completely obliterated by osmotic diuresis. In both experimental groups, a close relationship was observed between urine pH and the logarithm of the ratio between the urine and papillary concentrations of ammonia. The data are compatible with a proposal that a medullary countercurrent exchange system is responsible for medullary ammonia accumulation, and that diffusion equilibrium exists between the pNH3 of loop of Henle fluid, vasa recta blood, and collecting duct fluid.

A MICROPUNCTURE EVALUATION OF RENAL AMMONIA EXCRETION IN THE RAT.

Measurements of ammonia and inulin concentration were performed on samples of proximal or distal tubular fluid from 46 diuretic rats, some of which were pretreated with oral ammonium chloride. During mannitol diuresis alone, the ammonia concentration of midproximal tubular fluid averaged .77 ± .46 mm, while that of distal tubular fluid averaged 3.2 ± 1.1 mm. Midproximal ammonia was sufficient to account for as much as 62–70% of urine ammonia, while the distal tubular ammonia concentration theoretically provided 93–114%. After chronic ammonium chloride administration, the midproximal ammonia concentration rose to 1.5 ± .8 mm, while that of distal tubular fluid equaled 5.29 ± 1.3 mm. Net ammonia addition to collecting duct fluid was not obtained in either normal or acidotic rats. These observations demonstrate that the proximal tubule is an important potential source of final urine ammonia, and that increased proximal ammonia addition also occurs in response to chronic ammonium chloride acidosis. Although distal tubular ammonia addition probably occurs also, definite statements cannot be made regarding its magnitude in either normal or acidotic rats. However, it is apparent that the collecting duct is not an important source of final urine ammonia.

Influence of Diet on Urine Concentration in Aplodontia rufa and the Rabbit

UREA plays an important part in the production of a concentrated urine in mammals1. Berliner et al.2 postulate that urea contributes to the renal concentrating ability because it diffuses from the collecting ducts into the medullary interstitium and is trapped by capillary countercurrent exchangers, called vasa recta. Urea, therefore, increases the osmotic pressure of the medullary interstitial fluid with which the collecting duct fluid equilibrates during the formation of a hypertonic urine. Thus, increasing the available urea enhances maximum urine concentrating ability in most species which have been investigated (man, dog, rat, cat, kangaroo rat, and jerboa3)

The influence of vasopressin on the permeability of the mammalian collecting duct to urea.

The efficient operation of the renal concentrating mechanism is dependent tipon the action of vasopressin on the permeability of the distal convoluted tubule to water (1). In the presence of this hormone, hypotonic fluid entering the distal convolution equilibrates osmotically with fluid in the surrounding renal cortical tissue, and isotonicity of the fluid delivered to the collecting ducts is achieved (1, 2). The collecting ducts are surrounded by a medullary interstitium which is variably hyperosmolal to plasma (3-5). The osmotic movement of water from collecting duct lumen to medullary interstitium results in the excretion of a hypertonic urine. Despite evidence that movement of water across the collecting duct epithelium may occur in the apparent absence of vasopressin (6, 7), most schemes of the urinary concentrating process include the hypothesis that water permeability in this segment of the nephron is enhanced by this hormone. The present study was designed to test that hypothesis. Kinetic analysis of the action of vasopressin on the movement of water and solute across the toad skin indicates that the hormone acts to increase the pore size in this epithelial membrane (8, 9). If vasopressin exerts a similar action on the collecting duct epithelium, the permeability of the membrane to various partially permeant solutes should be affected by this agent. Since the urea concentration within the collecting duct fluid rises as water is abstracted from the lumen (10) it may be concluded that this membrane offers a barrier to the free diffusion of this molecule. It was therefore anticipated that an effect of vasopressin on the permeability of the collecting duct epithelial

Acute effects of brief ureteral stasis on urinary and renal papillary chloride concentration.

According to the countercurrent hypothesis urine tonicity depends largely on osmotic equilibrium of collecting duct fluid with the hypertonic interstitium of the papilla. One suggested role of ADH is that of regulating water permeability of collecting duct epithelium. In water deprivation ADH would facilitate water movement from collecting duct to the hypertonic papilla. Support for this hypothesis is offered here. These studies use the observation that ureteral clamping curtails glomerular filtration. Hence, the filtered load of NaCl from which papillary stores are derived is reduced. Accordingly, the chloride content of papillary tissues obtained from dog kidneys subsequent to several minutes of ureteral clamping was compared to those from the opposite kidney. In saline-loaded animals stasis uniformly lowered tissue chloride with the production of urine lower in chloride content and hypotonic to that of the contralateral side. These alterations were minimized following urinary stasis in animals loaded with water, mannitol or saline plus ADH.