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Query: UNIPROT:P41181 (collecting duct)
 5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During antidiuresis, the medullary collecting duct (MCD) reabsorbs sodium in load-dependent fashion. However, attempts to characterize reabsorption when sodium delivery to the MCD is elevated have not led to clear results, largely due to interfering effects of the strategies employed to raise delivery. In the present study, microcatheterization was performed in rats undergoing water diuresis induced solely by infusion of 2.5% dextrose in water, and in rats where solute delivery to the MCD was markedly elevated by the combination of water diuresis with acute potassium chloride loading. The results show that delivery of sodium was elevated by the experimental maneuvers, averaging 7.01 +/- 0.83 mumol . min-1 . g kidney wt-1 compared with a normal antidiuretic value in the literature of 3.50 +/- 0.40 mumol . min-1 . g-1. Sodium and chloride reabsorptions were increased proportionally, indicating that the MCD has a large capacity to transport sodium chloride. Normalized sodium reabsorption remained high, varying in different series between 80 +/- 10 and 96 +/- 1% of the delivered load. Thus the MCD reabsorbed an average of 6.37 +/- 0.70 mumol . min-1 . g-1 of sodium while sodium excretion was 0.52 +/- 0.11 mumol . min-1 . g-1. The results emphasize the importance of MCD sodium chloride reabsorption for determination of final urinary salt excretion, and thus for regulation of body salt balance.
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PMID:Load dependency of sodium chloride reabsorption by medullary collecting duct in rat. 366 17

These experiments were aimed at investigating renal behavior towards chloride, as distinct from sodium, during dietary deprivation of these ions in adrenalectomized rats. Adrenalectomized and shamoperated control rats were maintained on saline for 3 wk, then chloride conservation during a very low chloride intake was assessed both with an abundant sodium intake (as buffered sodium phosphate in the drinking water) and after subsequent withdrawal of sodium. When sodium intake was high, there was no difference in chloride conservation between adrenalectomized and control animals, and sodium balance and weight were maintained similarly in both groups. At the same time, both experimental and control rats developed significant hypokalemia and elevation of the plasma bicarbonate levels as compared to other control rats ingesting a normal diet. In another group of adrenalectomized rats sodium phosphate was withdrawn, after normal chloride conservation was observed, and the low-salt diet continued. Negative sodium balance developed and was associated with a negative chloride balance, whereas sham-operated rats continued to conserve sodium and chloride. In further studies during polyuria, both adrenalectomized and control rats developed urinary chloride concentrations of less than 1 meq/liter. Thus adrenalectomized rats can maintain chloride balance on a low chloride, high sodium intake, in contrast to their inability to conserve sodium on a low-sodium intake. It is concluded that renal tubular reabsorption of chloride in adrenalectomized rats is adequate to establish and maintain very low urinary chloride concentrations, which may imply active chloride transport in the papillary collecting duct despite the absence of adrenocortical hormone. In addition, the typical renal response to chloride deprivation, enhanced loss of potassium and accelerated reabsorption of bicarbonate, is not dependent on adrenocortical hormones.
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PMID:Effect of adrenalectomy on the renal response to chloride depletion in the rat. 443 35

Proximal and distal tubular function was compared with urinary excretion in rats after chronic administration of salt and deoxycorticosterone acetate (DOCA) or during salt deprivation. DOCA rats excreted significantly more sodium than did salt-deprived rats. Measurements of tubular fluid to plasma (TF/P) inulin ratios and concentrations of sodium and potassium in quantitative, timed collections, related to measured tubular length, allowed calculation of absolute reabsorption of fluid and ions in the different nephron segments. Proximal transport was not reduced in DOCA-treated rats compared with salt-deprived animals; in distal tubule the former group reabsorbed more sodium and secreted less potassium than the latter. Calculation of sodium transport in loop of Henle as the difference in flow between the end of the proximal convolution and the beginnings of the distal tubule indicated no inhibition of reabsorption in DOCA animals. Comparison of end-distal tubular flow with simultaneous urinary excretion suggested that sodium load was not the determining factor of enhanced natriuresis in DOCA-treated animals. The data are interpreted as indicating that DOCA-escape in the rat is associated with specific alteration of sodium transport in the collecting duct system.
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PMID:Proximal and distal tubular function in salt-deprived and in salt-loaded deoxycorticosterone acetate-escaped rats. 468 73

The analysis of the central core model of the renal medulla is extended to multisolute systems. It is shown that total solute concentration obeys the same differential equations for core and ascending limb as in a single solute system. Equations are derived for the concentration of individual solutes. Application of these equations to a two solute system shows that a central core system can concentrate with all transport being down a concentration gradient. This analysis applied to the renal medulla shows that mixing of urea from the collecting duct (CD) and salt from the loop of Henle in the central core of the inner medulla contributes to the concentration of urine during antidiuresis. It also sets criteria for completely passive function of the loop in the inner medulla, but whether these are satisfied cannot be determined from present experimental data.
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PMID:Concentrating engines and the kidney. II. Multisolute central core systems. 471 47

Hyperosmolality occurs when there are defects in the two major homeostatic mechanisms required for water balance-thirst and arginine vasopressin (AVP) release. In this situation hypotonic fluids are lost in substantial quantities causing depletion of both intracellular and extracellular fluid compartments. Patients with essential hypernatremia have defective osmotically stimulated AVP release and thirst but may have intact mechanisms for AVP release following hypovolemia. Hyperosmolality can also be seen in circumstances in which impermeable solutes are present in excessive quantities in extracellular fluid. Under these conditions there is cellular dehydration and the serum sodium may actually be reduced by water drawn out of cells along an osmotic gradient. Hyposmolality and hyponatremia may be seen in a variety of clinical conditions. Salt depletion, states in which edema occurs and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may all produce severe dilution of body fluids resulting in serious neurologic disturbances. The differential diagnosis of these states is greatly facilitated by careful clinical assessment of extracellular fluid volume and by determination of urine sodium concentration. Treatment of the hyposmolar syndromes is contingent on the pathophysiology of the underlying disorder; hyponatremia due to salt depletion is treated with infusions of isotonic saline whereas mild hyponatremia in cirrhosis and ascites is best treated with water restriction. Severe symptomatic hyponatremia due to SIADH is treated with hypertonic saline therapy, sometimes in association with intravenous administration of furosemide. Less severe, chronic cases may be treated with dichlormethyltetracycline which blocks the action of AVP on the collecting duct.
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PMID:The clinical physiology of water metabolism. Part III: The water depletion (hyperosmolar) and water excess (hyposmolar) syndromes. 624 83

Na-K-ATPase activity was measured in the convoluted part of the distal tubule (DCT), the connecting tubule (CNT) and the cortical collecting duct (CCD). The segments were microdissected from freeze-dried kidney tissue of rabbits adapted to various salt diets and exposed to large differences in endogenous and exogeneous mineralocorticoids. The Na-K-ATPase activity in the DCT is not influenced by mineralocorticoids. They do influence the activity in the CNT and in the CCD. In the CNT the highest activity was found with a low Na-, high K-diet. At the beginning of the CNT the enzyme activity is higher than in the end portion. While canrenoate-K treatment has no effect on Na-K-ATPase activity in the initial portions of the CNT, this drug decreases the Na-K-ATPase activity significantly in the end portion of the CNT. DOCA treatment has a significant effect on the enzyme activity in the CNT only in the end-portion of the segment, but provokes the highest Na-K-ATPase activity in the CCD. The changes in Na-K-ATPase are found to be associated with corresponding changes in the baso-lateral cell-membrane area in the segments affected.
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PMID:Distal tubular segments of the rabbit kidney after adaptation to altered Na- and K-intake. II. Changes in Na-K-ATPase activity. 628 47

Papillary necrosis, a common cause of renal failure, is a life-threatening pathophysiologic event which may have a multiplicity of mechanisms. The primary functional lesions are salt wastage, impairment of urinary concentrating ability, polyuria, and imbalances of potassium, calcium and phosphate homeostasis; urinary acidification is completely normal. Papillary necrosis is associated with a profound decrease in juxtamedullary nephron glomerular filtration rate, in addition to damage to the papillary collecting duct. 2-Bromoethylamine hydrobromide (BEA) has proved to be a useful tool in elucidating the generation of this important clinical syndrome.
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PMID:Pathophysiology of drug-induced papillary necrosis. 639 14

Diuretics have a central role in the treatment of edema and hypertension. This function is primarily an induction of a net negative balance of solute and water. Reviewed herein are the transport properties of each nephron segment that governs salt and water reabsorption with specific reference to the mechanisms by which the various diuretic agents affect those transport processes. Under normal circumstances, the proximal tubule reabsorbs about 50 to 66 percent of the filtered fluid by both active and passive mechanisms. However, diuretics that inhibit proximal reabsorption are "weak" diuretics since distal compensatory mechanisms can overcome their effect. The thin descending limb of Henle is highly permeable to water and relatively impermeable to solutes. Thus, its main physiologic function is to allow osmotic water abstraction. Although diuretics have no direct epithelial effect on this segment, many of the diuretics decrease fluid reabsorption from it by abolishing the papillary osmotic gradient. The decreased water absorption from the descending limb of Henle has a major role in over-all increased diuresis since nephron segments distal to the descending limb are impermeable to water in the absence of vasopressin. The thin ascending limb of Henle is impermeable to water while being highly permeable to sodium and chloride. Diuretics have no direct effect on the thin ascending limb of Henle. The medullary and cortical segments of the thick ascending limb of Henle absorb sodium chloride by active mechanisms as a result of a secondary active chloride transport mechanism that depends on the presence of sodium (co-transport mechanism). This transport mechanism is located on the luminal membrane. Most of the "loop" diuretics effect this process from the luminal side by having a direct inhibitory effect on this co-transport process. The diuretics that have a primary effect on the medullary segment (furosemide, bumetanide, ethacrynic acid) inhibit the concentrating mechanisms, whereas the diuretics that are effective primarily in the cortical segment (thiazides plus the diuretics affecting the medullary segment) inhibit the urinary diluting mechanism. The loop diuretics are physiologically the most potent family of diuretics. The cortical collecting duct segment reabsorbs sodium by active mechanisms. These processes are stimulated by aldosterone. The diuretics that affect these processes are considered weak diuretics, but they do have the metabolic effect of potassium sparing.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Site and mechanism of action of diuretics. 649 55

The renal medullary countercurrent system differentiates into its final segmental nephron function and geometry during perinatal development. The influence of these changes on the medullary longitudinal osmotic gradient cannot be evaluated by experimental studies. Therefore, a computation analysis using a differential equation model of the renal countercurrent system was applied to quantitate the effect of medullary architecture and solute transport on the concentration profiles for salt and urea in tubules (loop of Henle and collecting duct) and in the central core along the entire medulla during ontogeny. The results indicate that both the changing distribution of loop segments within the medulla and the increase in active salt transport of the individual thick ascending loop determine the magnitude and slope of the axial medullary solute gradients.
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PMID:Determinants of axial osmotic gradients in the differentiating countercurrent system. 669 14

The hypotheses of passive salt accumulation predict an enhancement of renal concentrating ability by urea. We tested this prediction in rabbits, a species whose nephons when studied in vitro show tansport properties that support these hypotheses. We used calm, unanesthetized, hydropenic, vasopressin-treated rabbits with intact kidneys fed a 16% protein diet, and we observed the effect of urea administration at two rates of solute excretion (60 and 190 microOsm/min . kg body wt; N = 10 and 5, respectively). After an i.v. mannitol infusion, when urea was infused, the i.v. solute excretion rate was unchanged, the changes in urine urea concentration were large (a change of 767 and 408 mumoles/ml), but only small and variable changes in urine osmolality occured (a change of 78 +/- 146, and 36 +/- 50 microOsm/g H20). In additional experiments, we removed the kidneys from antidiuretic, or urea- or mannitol-infused rabbits and measured the intrarenal distribution of sodium, potassium, urea, and chloride. When the urine urea level was greater than 400 mmoles, the urine-to-papilla ratios for urea were 1.6 to 3.6. This suggested that a low collecting duct permeability to urea could explain the absence of a marked enhancement of concentrating ability during urea administration. Further analysis, based on a model of inner medullary solute compartments, indicated that sodium chloride was the major (86%) osmotically active solute in the medullary central core of these rabbits and that it was not influenced by changes in urinary urea concentration. The results of tissue analysis were consonant with either active or passive sodium chloride reabsorption from the thin ascending limb of Henle's loop in these rabbits.
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PMID:Urea and renal concentrating ability in the rabbit. 677 Jan 67


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