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

The functions of a kidney, whether normal or cystic, can be conceptualized in terms of anatomy (glomerulus, proximal tubule, loop of Henle, distal convolution, and collecting duct), activity (volume regulation, dilution and concentration, acid-base regulation, potassium excretion, transport of organic molecules, and calcium and phosphate excretion), and the integration of anatomic organization to meet functional demand. Our discussion of renal cystic disorders follows this conceptual outline. For discussions of normal renal physiology, the reader is referred to any one of several recent, excellent reviews (1-3). Systematic evaluation of renal function in cystic diseases of the kidney (medullary sponge kidney, medullary cystic disease, and polycystic kidney disease) has only rarely been performed. The available information suggests that the earliest detectable lesions consist primarily of tubular dysfunction. With time, however, significant reduction of glomerular filtration occurs and the resultant accumulation of uremic toxins dominates the clinical picture in polycystic and medullary cystic disease. Significant changes in glomerular function are unusual in medullary sponge kidney. This review represents an attempt to summarize the large body of literature that has accumulated on functional abnormalities in these disorders, and to point out those areas where further investigations are needed.
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PMID:Functional abnormalities in renal cystic diseases. 0 65

Acute clearance studies were performed in normal subjects to assess the actions of the new diuretic, piretanide, on renal function. The drug increased both glomerular filtration rate and effective renal plasma flow in roughly proportionate amounts, so that filtration fraction did not change. In a dosage of 2 to 3 mg, it induced an increase in sodium excretion of almost 13% of filtered load, and there was an associated 2- to 3-fold increase in potassium excretion. The abstraction of solute-free water from the collecting duct was markedly reduced, but the drug induced no significant decline in the generation of free water. The rate of bicarbonate excretion, as well as that of titratable acid and ammonium, was increased approximately proportionately so that there was no increase in urinary pH or net hydrogen ion excretion. There was no phosphaturia, a unique finding, since all other drugs and maneuvers that cause a bicarbonate diuresis are also phosphaturic. Piretanide increased calcium excretion by approximately 19% of filtered load. The data suggest that the drug acts largely in the ascending limb of the loop of Henle and that it also affects the proximal tubule. Despite its sulfonamide structure, none of the drug's effects appear to be related to inhibition of carbonic anhydrase.
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PMID:Acute effects of piretanide in normal subjects. 3 85

Potassium depletion (KD) causes renal chloride-wasting. To investigate the effects of KD on renal tubular reabsorption of chloride, balance, clearance, micropuncture, and microinjection studies were performed on potassium-depleted rats. KD was produced by omitting potassium from the diet and by administration of DOCA on days 2 and 3; rats were studied on days 9 to 12. Diets were chloride-free in both control and KD groups. In the KD group, balance experiments confirmed greater chloride depletion and continued chloride-wasting, and clearance studies showed an increased FECl. Muscle potassium was reduced by 27% as compared to control. Whole kidney and single nephron GFR were reduced in KD rats to 72 and 74% of control. Fractional (6 +/- 6% vs. 22 +/- 4%, P less than 0.05) and absolute chloride reabsorption in the proximal tubule was not different. Fractional reabsorption of delivered chloride was reduced in the loop of Henle (92 +/- 0.8% in KD vs. 95 +/- 0.7% in control, P less than 0.02). Transtubular chloride ratio (0.28 +/- 0.02 vs. 0.21 +/- 0.02, P less than 0.02) was increased at the early distal tubule. Fractional delivery of chloride (8 +/- 0.9 vs. 5 +/- 0.5%, P less than 0.02), and fluid (26 +/- 1 vs. 22 +/- 1%, P less than 0.05) were also increased in KD at the early distal tubule. Recovery of chloride 36 injected into late distal tubules was 88 +/- 1% on a normal chloride intake, 62 +/- 2% in chloride depletion, and 88 +/- 2% in potassium and chloride depletion. Thus, KD depresses chloride reabsorption in the proximal tubule and in the loop of Henle, and it decreases chloride 36 efflux from the collecting duct.
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PMID:Effects of potassium depletion on renal tubular chloride transport in the rat. 3 45

Most of filtered K+ is reabsorbed passively in the proximal tubule since the tubular fluid (TF): plasma (P) concentration ratio is almost identical to the equilibrium value calculated from the transtubular potential difference. In the loop of Henle, K+ also moves passively along chemical and electrical gradients. Only 5-10% of the filtered K+ remains in the early distal convoluted tubule. In the distal convoluted tubule TF/P K+ is lower than the calculated equilibrium value suggesting that K+ is passively secreted and actively reabsorbed. Most of the excreted K+ had been secreted by the end of the distal convoluted tubule. Aldosterone increases K+ secretion in this segment, an effect that may be dissociated from the effect on Na+. The relation between K+ secretion and Na+ absorption is the consequence of the luminal electronegativity produced by Na+ absorption and is not stoichiometric. Acidosis and alkalosis decrease and increase K+ secretion in the distal tubule respectively; this is not due to reciprocal changes in H+ secretion. Normally, some K+ is reabsorbed in the collecting duct. During K+ deprivation and loading the collecting duct may participate in the conservation or elimination of K+ respectively. Adaptation to chronic K+-loading consists of renal and extrarenal factors. The extrarenal mechanism is aldosterone-dependent and consists of rapid uptake of K+ by muscle. The renal mechanism consists of increased K+ secretion by the distal tubule. Luminal electronegativity and increased K+ pool in the distal tubular cell play a crucial role.
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PMID:Disposition and regulation of body potassium: an overview. 13 35

The kidneys of a normal man filter approximately 24,000 meq sodium/day, reabsorb about 23,900, and yet can make a 1--2 meq change in 24-h urinary sodium excretion. The control of urinary sodium excretion, therefore, depends, first, on ensuring that the bulk of the sodium is reabsorbed, a function which is carried out in the proximal tubule and ascending loop of Henle. Second, it depends on adjusting the reabsorption of the small quantity of sodium which is delivered into the collecting duct so that the amount excreted in the urine is that required to maintain sodium balance. The bulk reabsorptive mechanisms can be considered as buffers to prevent large fluctuations in the amount of sodium delivered to the collecting duct, thus facilitating the fine adjustments of reabsorption which are made at this site. In conditions other than extreme salt loading or deprivation, changes in sodium reabsorption in the proximal tubule and loop of Henle probably have little, if any, effect on urinary sodium excretion. Sodium reabsorption in the proximal tubule and the collecting duct appears to be influenced by unidentified circulating substances.
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PMID:The control of sodium excretion. 35 40

Juxtamedullary (JM) nephron and collecting duct function was studied after a two-thirds reduction in renal mass in the young rat. The glomerular filtration rate of JM nephrons was twofold greater in the remnant kidney (RK) group than in controls, but this increase was proportional to the increase measured in surface nephrons. Despite an increase in absolute reabsorption, delivery of sodium and water to the end of the proximal tubule of superficial nephrons and to the bend of Henle's loop of JM nephrons was increased. This was a consequence of an increase in filtered load and a decrease in fractional reabsorption. Potassium handling in surface nephrons was similar to that of sodium and water. In deep nephrons of the RK group, potassium delivery to the bend was increased as a consequence of increased filtered load. The terminal portion of the collecting duct has a role in this adaptive response to a reduction in renal mass. In rats with a RK, reabsorption of water occurred along this segment; however, when the amount reabsorbed was related to delivery, fractional water reabsorption was only 30% of controls. Changes in sodium handling were more profound. In the group with the RK, sodium reabsorption was not detectable along this segment. Thus, while 40% of delivered sodium was reabsorbed in controls, in the remnant kidney group the mean was not different from zero (-1.7%).
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PMID:Response of deep nephrons and the terminal collecting duct to a reduction in renal mass. 44 83

Dogs are frequent subjects in experimental studies of renal physiology and pathology in spite of the paucity of information on their normal renal morphology. In this study, gross morphology, light microscopy, and scanning and transmission electron microscopy were used to describe dog renal anatomy. The dog has a multilobed kidney with the medulla fused into an elongate crest and a renal pelvis of elaborate shape. The outer zone of the medulla lacks a definitive outer stripe. The proximal tubule consists of four distinct anatomical segments. Dark cells are abundant in the collecting duct of the inner medulla. The majority of the nephron segments demonstrate remarkable similarities to those of the human kidney and less to those of the kidney of the laboratory rat.
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PMID:Survey of the morphology of the dog kidney. 44 63

Prostaglandins have been postulated to participate in the regulation of salt excretion during acute volume expansion. The present papillary and cortical micropuncture studies were designed to examine the effect of prostaglandin synthesis inhibitors on segmental chloride transport during hydropenia (with and without meclofenamate) and 10% volume expansion (with and without both meclofenamate and indomethacin). Both inhibitors significantly decreased the urinary excretion rate of prostaglandins E(2) and F(2alpha). Clearance studies on the intact right kidney demonstrated no effect of either agent on glomerular filtration rate, but a significant reduction in chloride excretion during hydropenia and volume expansion was observed. To assess the specific site(s) of enhanced chloride reabsorption, absolute and fractional chloride delivery was measured in the late proximal tubule, thin descending limb of Henle, and the early and late distal tubules. In addition, the fraction of filtered chloride remaining at the base and tip of the papillary collecting duct was compared to that fraction remaining at the superficial late distal tubule. During hydropenia, meclofenamate had no effect on fractional chloride delivery out of the superficial late distal tubule or the juxtamedullary thin descending limb of Henle, but significantly reduced the fraction of chloride delivered to the base of the papillary collecting duct. During volume expansion, neither meclofenamate nor indomethacin had an effect on absolute chloride delivery out of the proximal tubule or the thin descending limb of Henle. However, absolute chloride delivery to the early distal tubule was significantly reduced, and was associated with a decrease in fractional chloride reabsorption in this segment. Furthermore, the fraction of chloride delivered to the base of the collecting duct was significantly reduced. Fractional reabsorption along the terminal 1 mm of the collecting duct was not altered by either meclofenamate or indomethacin. These results suggest that inhibitors of prostaglandin synthesis result in an increase in chloride reabsorption in the superficial loop of Henle, and in segments between the superficial late distal tubule and the base of the collecting duct. The results are consistent with the view that prostaglandins inhibit chloride transport in the thick ascending limb of Henle, and/or the cortical and outer medullary collecting tubule.
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PMID:Cortical and papillary micropuncture examination of chloride transport in segments of the rat kidney during inhibition of prostaglandin production. Possible role for prostaglandins in the chloruresis of acute volume expansion. 50 Aug 11

Superficial proximal and distal tubules of both kidneys of pentobarbital-anesthetized cats, infused with 2.5% (w/v) polyfructosan in Ringer solution at 0.45 ml/min, were micropunctured. Whole one-kidney GFR average 4.1 ml/min. SNGFR averaged 15 nl/min in 51 determinations and was proportional to whole-kidney GFR in individual cats. Absolute fluid reabsorption along the length of the accessible portion of the proximal tubule was 1.6 nl/min.mm. The length of the whole proximal tubule was 6 mm as measured from the glomerulum to the descending thin limb of Henle's loop. The length of the distal tubule was 3.5 mm from the macula densa to the first branching of the collecting duct. Proximal fluid was isoosmolar with plasma whereas fluid entering the distal tubule was markedly hyposmolar. Late distal tubular fluid samples were also isosmolar. The cat appears to be well suited for micropuncture experiments in terms of freedom from respiratory movements and the presence of surface distal tubules.
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PMID:Micropuncture study of fluid handling in the cat kidney. 56 46

In a recent study it was found that in Mg loaded rats, the fraction of filtered Mg (% E Mg) recovered in the bend of the loop of Henle of papilla was greater than the filtered load. However, the site of this Mg addition was unspecified and could be either the juxtamedullary proximal tubule, the pars recta, or in the papilla, the descending limb of the loop of Henle. In order to investigate the movement of Mg in the various structures of the papilla, we have studied: 1. The transport of this electrolyte along the collecting duct. 2. Its relative concentration in the loop of Henle and in the adjacent vasa recta. The experiments have been performed in hydropenic and Mg loaded rats. In the collecting duct, the inulin and Mg concentrations increase proportionally, indicating an absence of any transport of Mg along this part of this nephron. In the vasa recta of the accessible papilla, the capillary over peripheral plasma Mg ratio (C/UF Mg) in hydropenia and after Mg loading [1.88 +/- 0.15 (ES) and 2.89 +/- 0.25] were significantly lower than the corresponding TF/UF Mg in the adjacent loops of Henle (2.90 +/- 0.17 and 4.04 +/- 0.37). This finding reduces the possibilities of a Mg passive diffusion from the capillaries to the tubular lumen, unless the electrical potential of the descending limb is more negative than -5 mV. The hypothesis of an active secretion, or a passive diffusion of Mg in the deep proximal tubule, in the pars recta, or in the early non accessible descending limb constitutes the other alternative.
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PMID:Magnesium handling by the papilla of the young rat. 56 20


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