Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P41181 (collecting duct)
5,183 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal micropuncture and microdissection techniques with ultramicro fluid analysis have been applied to evaluate single nephron function in the skate, Raja erinacea. We have divided the skate nephron into three proximal tubular segments (PTS I-III), three distal coilings (DC I-III), and a countercurrent loop system located between the proximal segments and the distal coilings. The collecting duct is the principal site of urinary dilution. Following exposure of the fish to 75% seawater for about 24 hours, the sodium concentration difference between the end collecting duct lumen and plasma is decreased sufficiently to account for the urinary dilution. The principal site for magnesium, phosphate and sulphate secretion appears to be PTS II. This segment is located on the ventral surface of the kidney. PTS II is also the main nephron site for reabsorption of sodium and chloride in excess of water.
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PMID:Renal tubule ion transport and collecting duct function in the elasmobranch little skate, Raja erinacea. 85 Jan 20

The effects of acute bilateral ureteral obstruction (BUO) of 18-h duration on deep nephron and collecting duct function were studied by micropuncture in 11 weanling rats. After release of BUO glomerular filtration rate was reduced (178+/-15 vs. 1,343+/-119 mul/min per g kidney weight in shams), while urine flow was increased averaging 17.5+/-1.3 vs. 6.8+/-0.72 mul/min per g kidney weight in controls. There was a marked increase in the absolute and fractional excretion of Na. Single nephron glomerular filtration rate of deep nephrons was reduced in the BUO group, mean 19.4+/-3.5 vs. 77.0+/-7.7 nl/min per g kidney weight in shams. Single nephron glomerular filtration rate of superficial nephrons fell to the same extent after relief of BUO. Mean tubular fluid to plasma inulin ratio of fluid from Henle's loop was 2.46+/-0.20 after relief of BUO vs. 8.23+/-0.85 in shams. This suggested a reduction in the reabsorption of Na and water before the bend of the loop of Henle, most likely in both the proximal tubule and descending limb. Fluid osmolality was depressed due to a decline in both Na and nonelectrolyte solute content. After release of BUO the percentage of filtered water remaining in the collecting duct (CD) at the base of the papilla was greater than in controls (13.3+/-2.0 and 1.72+/-0.01%, respectively) but fell significantly by the tip of the papilla to 7.92+/-1.12 vs. 1.17+/-0.02% in controls. These results indicate that water was reabsorbed along the terminal CD after relief of ureteral obstruction. In fact, a greater fraction was reabsorbed in this segment after release of BUO (5.37+/-1.58%) than after sham operation (0.55+/-0.15%). Similar changes were seen in Na excretion. Thus alterations in deep nephron function appear to contribute to the natriuresis and diuresis which follow release of BUO while terminal CD function in this model appears intact.
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PMID:Effects of acute bilateral ureteral obstruction on deep nephron and terminal collecting duct function in the young rat. 86 2

Thirty minutes after indomethacin (10 mg/kg, iv), a prostaglandin synthesis inhibitor, had been given to 10 rats, the Na concentration in renal papilla averaged 349 mEq/kg H2O, whereas it averaged only 181 in 14 "non-indomethacin" control rats (P less than 0.0001). Papillary plasma flow was closely similar in both groups. In a subsequent study, eight "indomethacin" rats had the same papillary flow as seven non-indomethacin rats but had a papillary Na concentration of 358 vs. 185 in the non-indomethacin controls (P less than 0.0001). In nine more rats, indomethacin increased Cl concentration in papillas by 66% (P less than 0.0001), while Na concentration increased 60% (P less than 0.0001). In eight other rats, micropuncture indicated that indomethacin does not greatly alter delivery of fluid out of late proximal tubule. Meclofenamate, another inhibitor, increased papillary Na just as much as indomethacin. Papillary urea is not changed with indomethacin. Thus, papillary Na concentration was almost twice as high in indomethacin rats, despite similar papillary plasma flow and late proximal flow. Apparently, inhibiting prostaglandin synthesis is associated with either a great increase in Na or Cl "pumping" or a great decrease in Na or Cl "leak" in either collecting duct or ascending limb, or in both. The collecting duct and papillary interstitial cells both synthesize prostaglandins, which seem to have a profound effect on medullary net Na transport.
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PMID:Evidence that prostaglandin synthesis inhibitors increase the concentration of sodium and chloride in rat renal medulla. 87 Feb 22

1. Antidiuretic hormone (ADH) was infused into normal male rats at a rate of 60 muu./min. 100 g body wt., to maintain an effectively constant maximal circulating level. Four groups of rats were used; they were water-loaded by receiving together with the ADH, I.V. infusions of hypotonic dextrose (2.5 g/100 ml.) at different rates (1.0, 4.5, 9.0 and 12 ml./hr, respectively), over an infusion period of 4 hr.2. Urine flow rate increased in all groups, the rate and extent of the increase being related to the volume rate of infusion. The differences in urine flow rates between the four groups were due almost entirely to increases in free water clearance, with no consistent differences in osmolal clearance between the groups. At the end of the 4 hr infusion period, osmolal clearances were closely similar in the four groups.3. Papillary and medullary tissue solute concentrations were progressively reduced at the higher rates of infusion. The changes were due to small increases in the water content, together with a profound decrease in urea concentration and a smaller decrease in sodium concentration. However, papillary osmolality was consistently higher than urine osmolality at the three highest rates of dextrose infusion.4. As urine flow rate increased, there was a progressive reduction in the degree of osmotic equilibration between the final urine and the papillary tip. For urea, however, the degree of equilibration remained high.5. It is concluded that, in the rat, the rate of flow per se, along the collecting duct, is an important determinant of final urine concentration; even if there is an osmotic driving force for water re-absorption in the renal medulla, and the collecting duct walls are permeable to water, osmotic equilibration is restricted by tubular flow rate.
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PMID:Collecting duct dlow rate as a determinant of equilibration between urine and renal papilla in the rat in the presence of a maximal antidiuretic hormone concentration. 90 5

Medullary collecting duct function was studied by direct microcatheterization techniques in rats undergoing postobstructive diuresis. Significant net addition of water and sodium to the duct was demonstrated during postobstructive diuresis after relief of 24-h bilateral ureteral ligation. This striking abnormality in function was associated with reduced delivery of sodium and water to the collecting duct compared to sham-operated controls. To examine the role of circulating factors in this phenomenon, another group of rats was studied that underwent 24 h of total urine reinfusion into the femoral vein. Natriuresis and diuresis were similar to the postobstructive group, but absolute collecting duct reabsorption of sodium and water was normal. The natriuresis and diuresis in rats with urine reinfusion resulted from increased delivery of fluid and sodium to the medullary collecting duct. A third group of rats was studied with 24-h unilateral ureteral ligation as well as urine reinfusion from the contralateral normal kidney. Without urine reinfusion there was no diuresis-natriuresis but with urine reinfusion the diuresis and natriuresis after relief of unilateral obstruction was similar to that after relief of bilateral obstruction. Moreover, net addition of sodium and no significant water reabsorption were demonstrated in the medullary collecting duct of such animals. The results indicate that (a) the medullary collecting duct is the critical nephron segment affected by ureteral obstruction, since postobstructive diuresis occurred despite reduced delivery of fluid from the more proximal nephron; (b) the net addition of sodium to the medullary collecting duct observed during postobstructive diuresis is probably a direct effect of obstruction, since it was found during postobstructive diuresis after relief of bilateral or unilateral ureteral ligation, but not with urine reinfusion alone; and (c) blood-borne factors are important in the development of postobstructive natriuresis and diuresis, and probably act by increasing the fraction of filtered sodium and water delivered from the proximal and distal tubule to the collecting duct.
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PMID:The role of the medullary collecting ducts in postobstructive diuresis. 93 94

The effects of furosemide were studied on isolated dog kidneys in the absence and in the presence of vasopressin. In the latter condition, furosemide did not modify renal blood flow and glomerular filtration rate while both parameters were decreased by the drug in the absence of vasopressin, as they were also reduced by vasopressin alone. This would indicate direct vasoactive effects of furosemide, depending on the previous tone of the vasculature. In the absence of vasopressin, furosemide decreased free water clearance through inhibition of sodium reabsorption in the ascending limb of Henle's loop. On the other hand, in the presence of vasopressin, furosemide increased free water clearance, presumably through reduction of water reabsorption in the collecting duct by enhanced distal tubular flux.
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PMID:Interactions between furosemide and vasopressin on hemodynamics and on water excretion by the isolated dog kidney. 94 35

The effects of acute hypercalcemia on hemodynamics and on water and sodium excretion were studied on the blood-perfused isolated dog kidney. This model advantageously eliminates various factors which modify medullary osmolality and intrarenal hemodynamics, as well as collecting duct permeability. Calcium ion directly inhibits sodium reabsorption in the proximal tubule and in the ascending limb of Henle's loop, leading to increased sodium excretion rate and to decreased free water generation. The vasoconstrictive action of calcium, leading to decreased glomerular filtration rate, may mitigate the strong natriuretic effect of this ion.
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PMID:Effects of hypercalcemia on water and sodium excretion by the isolated dog kidney. 94 13

The effect of injections of ovine prolactin on kidney structure was examined in the first 10 days following transfer of seawater sticklebacks to fresh water. In hormone injected animals as well as in controls the glomeruli increase slightly in size after transfer. The podocytes intensify the secretion of mucopolysaccharides, which is indicative of increased turnover of the components of the glomerular basal lamina. The nuclei of the podocytes become enlarged, while those of the juxtaglomerular cells decrease in size. These changes are related to the well known rise of the glomerular filtration rate following transfer to fresh water. Structural indications that prolactin is involved in the control of glomerular filtration were not found. The epithelial cells of the three nephronic segments and of the ureter become considerably better developed after transfer to fresh water. Cell height, nuclear and mitochondrial volume, and surface of the membranes of the basal labyrinth increase in all tubular epithelia, although not to the same extent. Increases are moderate in the first proximal segment, but increasingly higher for the second proximal segment, collecting duct and the ureter. Especially the growth of membrane surface of the basal labyrinth, site of ion transport mechanisms, is impressive. In controls, values characteristic for freshwater fishes are reached in 6 to 9 days for all parameters for cellular development. Prolactin injections greatly stimulate growth rates in all tubular epithelia: freshwater values are reached within 3 days. No further increase was found, however.
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PMID:The effect of prolactin on kidney structure of the euryhaline teleost Gasterosteus aculeatus during adaptation to fresh water. 94 16

The administration of diphenylamine to rats induces an acquired form of cystic disease. In order to examine the early changes in this model of experimental cystic disease prior to the development of the more severe structural alterations, clearance, micropuncture, and morphologic studies were performed in rats fed DPA for 3 to 6 weeks. A significant defect in maximal urine concentrating ability (Umax) was manifest by the second week and averaged 50% of control values. Further studies were undertaken to examine the cause of the defect in Umax. Whole-kidney glomerular filtration rate (GFR), single-nephron GFR, end-proximal TF/Pinulin, glucose and bicarbonate reabsorption were all normal, indicating normal function of the proximal tubule. Free water clearance and free water reabsorption were not significantly different in DPA-treated rats as compared to controls, suggesting normal function of the ascending limb of the loop of Henle and collecting duct. Morphologic examination revealed gross cysts in less than 10% of the kidneys but structural changes were consistently demonstrated in the collecting ducts of DPA-treated rats. These studies indicate that the decrease in Umax in DPA-treated animals is the result of a defect located at the terminal portion of the collecting duct.
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PMID:Renal function in experimental cystic disease of the rat. 95 92

Although chronic lithium therapy has been associated with a defect in the urinary concentrating mechanism, short-term renal effects of lithium have received little attention in the intact animal. Solute-free water reabsorption (T-cH2O) and free water clearance (CH2O) were measured in primates of the genus Galago under control conditions and while animals were receiving either 0.5 mmol/kg-h or 1.0 mmol/kg-h lithium chloride (135 mM) intravenously. CH2O was unchanged by lithium infusion (P greater than 0.10), whereas T-cH2O was significantly depressed at all levels of osmolal clearance (P smaller than 0.01). Spontaneous recovery of near-normal T-cH2O was documented in two animals within 1 wk following acute lithium infusion. In addition it was observed that lithium-induced depression of T-cH2O could be partially prevented by pretreatment with intravenous amiloride. These results suggest that alterations in the renal concentrating mechanism can occur rapidly following the onset of lithium administration. They also imply that impairment of the renal concentrating mechanism by lithium is due at least in part to antagonism of the action of vasopressin on the collecting duct.
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PMID:Acute effects of lithium on the renal concentrating mechanism in a primate. 111 55


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