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

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

In order to study the mechanism of enhanced potassium excretion by the remaining nephrons of the remnant kidney, micropuncture and clearance experiments were carried out in rats after surgical ablation of 3/4 of the total renal mass. The potassium intake in all animals was approximately 5 meq/day. Animals were studied 24 h and 10-14 days after 3/4 nephrectomy. Balance measurements in the chronic animals before micropuncture study indicated that 24 h K(+) excretion by the remnant kidney was equal to that of the two kidneys before ablation of renal mass. Measurements of distal tubular inulin and potassium concentrations revealed progressive reabsorption of potassium in this segment of the nephron in both the 24-h and chronic 3/4-nephrectomized rats, as well as in normal control rats. A large increase in tubular fluid potassium content occurred between the end of the distal tubule and the final urine in the 3/4-nephrectomized rats, but not in the normal controls. These observations suggest that the segment of the nephron responsible for enhanced potassium excretion by remaining nephrons was the collecting duct. In additional experiments, potassium was completely eliminated from the diet of chronic 3/4-nephrectomized rats before micropuncture study. In these animals, no addition of K(+) occurred beyond the distal tubules. Normal rats infused with 0.15 M KCl to acutely elevate serum K(+) concentration, demonstrated reabsorption of K(+) in the distal tubule and a large addition of K(+) to the urine beyond the distal tubule. We conclude that the collecting duct is the major site of regulation of urinary potassium excretion in normal rats and is responsible for the adaptation to nephron loss by the remnant kidney.
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PMID:A micropuncture study of potassium excretion by the remnant kidney. 470 32

1. The time course and extent of changes in the composition of renal tissue slices in osmotic diuresis were determined by sacrificing groups of rats before and during the intravenous infusion of mannitol (15 g/100 ml.) for up to 7(1/2) hr.2. Very rapid changes in tissue water and solute contents occurred within 15 min, preceding the times of maximal diuresis, with little subsequent change even up to 7(1/2) hr.3. The main changes were:(a) an increase in water content in all slices, particularly the papilla; (b) a very profound decrease in papillary and medullary urea content in the first 15 min, with a small, but significant, further decrease, subsequently; (c) a small, but significant, rapid decrease in papillary sodium, and small non-significant increases in the outer medulla and cortex. Subsequent changes in any segment were small and non-significant; (d) apart from small changes in the first 15 min ammonium and potassium contents remained fairly constant.4. The rates of change in papillary and urinary urea concentrations were similar, so that after 30 min, any differences between tip and urinary concentrations were small and non-significant.5. The findings are discussed in terms of factors influencing counter-current mechanisms. It is concluded that altered medullary blood flow is mainly responsible for the rapid changes in medullary composition.6. The relation between papillary and urinary urea concentrations is explicable in terms of passive handling, with equilibration across a freely permeable collecting duct membrane.
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PMID:The time course of changes in renal tissue composition during mannitol diuresis in the rat. 571 51

Microelectrode techniques were applied to the rabbit isolated perfused cortical collecting duct to provide an initial quantitation and characterization of the cell membrane and tight junction conductances. Initial studies demonstrated that the fractional resistance (ratio of the resistance of the apical cell membrane to the sum of the resistances of the apical and basolateral membranes) was usually independent of the point along the tubule of microelectrode impalement--implicating little cell-to-cell coupling--supporting the application of quantitative techniques to the cortical collecting duct. It was demonstrated that in the presence of amiloride, either reduction in the luminal pH or the addition of barium to the perfusate selectively reduced the apical membrane potassium conductance. From the changes in Gte and fractional resistance upon reducing the luminal pH or addition of barium to the perfusate, the transepithelial, apical membrane, basolateral membrane and tight junction conductances were estimated to be 9.3, 6.7, 8.1 and 6.0 mS cm-2, respectively. Ninety to ninety-five percent of the apical membrane conductance reflected the barium-sensitive potassium conductance in the presence of amiloride with an estimated potassium permeability of 1.1 X 10(-4) cm sec-1. Reduction in the perfusate pH to 4.0 caused a 70% decrease in the apical membrane potassium conductance, implying a blocking site with an acidic group having a pKa near 4.4. It is concluded that both the transcellular and paracellular pathways of the cortical collecting tubule have high ionic conductances, and that the apical membrane conductance primarily reflects a high potassium conductance. Furthermore, both reduction in the perfusate pH and addition of barium to the perfusate selectively block the apical potassium channels, although the site of inhibition likely differs since the two ions display markedly different voltage-dependent blocks of the channel.
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PMID:Electrophysiological properties of cellular and paracellular conductive pathways of the rabbit cortical collecting duct. 609 25

Studies were performed on the initial collecting tubule of the rat to determine whether potassium adaptation in this nephron segment is aldosterone-dependent. Previous studies demonstrated that chronic potassium loading, in animals with intact adrenal glands, caused an increase in transepithelial potential difference in late distal convolution, an increase in surface density of the basolateral cell membrane, SVBLM, of principal cells in the initial collecting duct, and a rise in plasma aldosterone levels. The present study shows that epithelial changes that characterize dietary potassium loading are not dependent on hyperaldosteronism, since potential difference (-47 +/- 1 vs. 40 +/- 3 mV, lumen negative) and SVBLM (2.91 +/- 0.11 vs. 2.53 +/- 0.09 micron2/micron3) increased significantly (P less than 0.05) in the late distal convolution of adrenalectomized, hormone-replaced animals in which plasma aldosterone levels were maintained at basal values of approximately 5 ng/dl. In addition, these experiments suggest that the initial collecting tubule is sensitive to the action of aldosterone, at physiological plasma levels, since chronic hyperaldosteronism, in the absence of potassium loading, increased SVBLM in initial collecting tubule cells. In contrast to other mineralocorticoid-sensitive tissues, however, neither the acute or chronic administration of aldosterone caused an increase in potential difference in late distal convolution. These results suggest that the mechanism by which aldosterone stimulates electrolyte movement is not identical in all target tissues.
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PMID:Role of aldosterone in the mechanism of potassium adaptation in the initial collecting tubule. 609 57

Chronic potassium loading results in an increased capacity of the distal nephron to secrete potassium. The cellular mechanism for this adaptation has been correlated to an increase in the activity of sodium-potassium-ATPase. Because adaptation may be dependent on the greater availability of potassium pumps in the basolateral membrane, a stereologic analysis of the membrane surface area was performed to determine whether the apparent increase in pump sites was due to an increase in cell membrane surface. With potssium adaptation, the number of microplicated cells in the outer medulla was reduced from 31 to 18%. There was a marked increase in the basolateral infolding of principal cells, and membrane surface increased by 32%. In papillary collecting duct cells, the basolateral membrane surface was unchanged but the surface density of the luminal membrane increased by 50%. These observations suggest that amplification of the basolateral cell membrane to increase the number of potassium pump sites per cell plays an important role in the mechanism of potassium adaptation in the outer medulla. A different mechanism involving the luminal membrane operates in the papillary collecting duct. Structural alterations in cell membrane surfaces are thus related to the regulation of the epithelial transport of electrolytes.
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PMID:Changes in membrane surfaces of collecting duct cells in potassium adaptation. 625 63

Potassium excreted by the kidney is derived largely from potassium secretion by the distal tubule and collecting duct. It is this secreted fraction that responds to systemic changes and is mainly responsible for regulation of potassium balance. A smaller fraction of the excreted quantity comes from potassium that is filtered and escapes reabsorption. Variations in the rate of reabsorption may alter potassium secretion under some circumstances. In the proximal tubule, reabsorption of potassium appears to involve interaction with a membrane mechanism. The contribution of descending limb potassium secretion to final potassium secretion is a present uncertain because of the inaccessibility of inner cortical distal tubules and collecting ducts in intact animals. Changes in plasma K, plasma aldosterone, and plasma acidity all appear to affect distal potassium secretion by influencing the uptake of potassium from blood to cell and thus raising the intracellular potassium. Changes in extracellular fluid volume, which increase urine flow and sodium excretion, appear to increase distal potassium secretion as a consequence of increases in the flow rate of luminal fluid. Flow-dependent changes in luminal potassium concentration may be involved but they do not appear to act by simply increasing the passive electrochemical driving force (assessed across the entire epithelium). Our understanding of the cellular mechanisms controlling renal potassium secretion is becoming clearer as it becomes possible to identify and to separate for a study a potentially confusing array of interacting variables.
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PMID:Potassium transport by successive segments of the mammalian nephron. 626 88

In this review, the distal nephron is considered to be that portion of the renal tubule commencing with the thick ascending limb of the loop of Henle and ending with the papillary collecting duct. The collecting duct, including its subdivisions in the cortex and medulla, originates from a different embryologic anlage than more proximal nephron segments, which may explain its morphologic and functional dissimilarities from the thick ascending limb and the distal convoluted tubule. This review summarizes selected aspects of the physiology of the distal nephron, with particular emphasis on the physiology of distal nephron transport of sodium, potassium, chloride and hydrogen ion. The pathophysiologic features of the following disorders of distal nephron function are reviewed: (1) pseudohypoaldosteronism, a heterogenous group of disorders in which the signs and symptoms are suggestive of aldosterone deficiency, but in which aldosterone levels are supernormal and administration of exogenous mineralocorticoid is not ameliorative; (2) pseudohyperaldosteronism (Liddle syndrome), a familial disorder in which the clinical manifestations closely resemble those resulting from an aldosterone-producing adenoma of the adrenal gland (primary aldosteronism), but in which the measured rate of aldosterone secretion and excretion is greatly subnormal; (3) Bartter syndrome and related syndromes of renal potassium wasting; (4) type 1 renal tubular acidosis (classic, distal); (5) type 4 renal tubular acidosis (hyperkalemic). Reference citations are generally to articles reporting recent advances in these areas and to review articles that contain comprehensive bibliographies.
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PMID:Disorders of distal nephron function. 627 92

Na-K-ATPase activity was determined in 10 segments of the rat nephron using a fluorometric microassay method [4]. The enzyme activity showed three peaks (greater than 200 pmol ADP min-1 mm-1) along the nephron of normal rats. These peaks were in the S1 portion of the proximal tubule, the medullary thick ascending limb from the inner stripe and the distal convoluted tubule. Feeding the rats a low potassium diet for 8 weeks produced a significant decrease in Na-K-ATPase activity in the cortical collecting duct, but no significant change in this enzyme in any other segment. The low potassium diet did not produce a significant change in Mg-ATPase in any nephron segments. We conclude that Na-K-ATPase activity along the rat nephron shows a pattern that is qualitatively similar to that seen in the rabbit nephron [4]. However, quantitatively the Na-K-ATPase activity in the rat nephron is greater than in the corresponding segments of the rabbit nephron. The results are consistent with the greater rate of glomerular filtration and Na+ reabsorption per rat nephron. Furthermore, our results suggest that the decrease in potassium excretion during potassium deficiency is modulated, at least in part, by the level of Na-K-ATPase activity in the cortical collecting duct.
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PMID:Effect of low potassium-diet on Na-K-ATPase in rat nephron segments. 628 58

The criteria upon which diuretics are classified is based upon their site of action within the nephron. Carboanhydrase inhibitors act in the proximal tubule, high-ceiling diuretics in the ascending loop of Henle, the thiazides in the early distal tubule and the potassium-sparing diuretics in the late distal tubule and in the collecting duct. On the molecular level diuretics do not inhibit Na+-K+-ATPase but interfere with the permeability of the tubule membranes or transport systems for certain ions and thus also influence the potential differences in the different parts of the nephron. Since carboanhydrase is located in the proximal tubule cells, not only in the cytosol but also in the brushborders and in the peritubular membranes, acetazolamide and other carboanhydrase inhibitors act on three different sites in these cells. The loop diuretics inhibit the secondary active chloride reabsorption. The receptors in this part of the nephron are stereospecific. Only the levorotatory isomere of ozolinone has active diuretic properties whereas the dextrorotatory isomere does not. Perfusion experiments of the loop of Henle with different lectins give evidence that glycoproteins containing alpha-1-fucose are involved in the reabsorption of Na+ and Cl-. Experiments on the isolated stripped rabbit colon under the condition of chloride secretion reveal striking similarities between the receptors for chloride reabsorption in the luminal cell membranes of the ascending loop of Henle and in the serosal cell membranes of the colon. The potassium-sparing diuretics amiloride and triamterene act by blocking sodium channels in the distal parts of the nephron. Thus the lumen negative potential difference decreases and (passive) potassium secretion is diminished.
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PMID:Molecular actions of diuretics. 629 72


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