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)

Vasopressin is known to increase the permeability of the toad bladder, an analogue of the mammalian collecting duct, to water and hydrophilic solutes such as urea. In the present study, the effect of vasopressin on the permeability of a series of lipophilic compounds, including many commonly used drugs, has been determined. In all cases, permeability increased from 50 to 100%. The response to vasopressin was mediated by cyclic adenosine monophosphate (cAMP), and was generally not altered by phloretin, an agent that inhibits amide movement through the amide transport pathway. Evidence that these compounds move directly through the lipid phase of the membrane was provided in studies of phenobarbital permeability at low and high luminal pH. We would conclude from these studies that the effect of vasopressin on the luminal cell membrane is a widespread one, modifying both lipid components and components involved in amide, sodium and water transport. This may be of importance in the renal tubular reabsorption of many drugs, including barbiturates, glutethimide and antibiotics.
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PMID:Vasopressin-stimulated movement of drugs and uric acid across the toad urinary bladder. 0 5

1. The proposition that changes in renal calcium excretion during vasopressin administration are positively correlated with concurrent changes in urine hydrogen ion concentration was tested by administration of vasopressin into twelve conscious diuresing sheep receiving either alkalinizing or acidifying infusions. 2. Vasopressin-induced antidiuresis in sheep with alkaline urine was associated with significant increases in urinary pH and decreases in the rate of calcium excretion whereas antidiuresis in sheep with acid urine was associated with significant decreases in urinary pH and no consistent effect on calcium excretion. 3. Magnesium excretion increased during vasopressin administration in most experiments regardless of urinary pH changes. 4. Vasopressin administration did not significantly alter the rate of excretion of sodium, potassium, chloride and phosphate or the rates of sodium, potassium, chloride, inulin, para-aminohippurate and osmolal clearance in sheep with either acid or alkaline urine. Potassium excretion and clearance in sheep with alkaline ruine was higher than that of sheep with acid urine during vasopressin infusion. 5. The results support the hypothesis that changes in renal tubular hydrogen ion concentration or bicarbonate concentration caused by water reabsorption from the collecting duct and possibly the late distal tubule could be part of the explanation for changes in renal calcium excretion which occur during vasopressin-induced antidiuresis.
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PMID:Renal calcium and magnesium excretion during vasopressin administration into sheep with acid or alkaline urine. 4 39

Vasopressin increases the permeability of the total urinary bladder, an analogue of the mammalian renal collecting duct, to water and small solutes, especially the amide urea. We have observed that three general anesthetic agents of clinical importance, the gases methoxyflurane and halothane and the ultrashortacting barbiturate methohexital, reversibly inhibit vasopressin-stimulated water flow, but do not depress permeability to urea, or the the lipophilic solute diphenylhydantoin. In contrast to their effects in vasopressin-treated bladders, the anesthetics do not inhibit cyclic AMP-stimulated water flow, consistent with an effect on vasopressin-responsive adenylate cyclase. The selectivity of the anesthetic-induced depression of water flow suggests that separate adenylate cyclases and cyclic AMP pools may exist for control of water and urea permeabilities in to toad bladder. Furthermore, theophylline's usual stimulatory effect on water flow, but not its effect on urea permeability, was entirely abolished in methoxyflurane-treated bladders, suggesting that separate phosphodiesterases that control water and urea permeabilities are present as well. We conclude that the majority of water and urea transport takes place via separate pathways across the rate-limiting luminal membrane of the bladder cell, and that separate vasopressin-responsive cellular pools of cyclic AMP appear to control permeability to water and to urea.
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PMID:Selective inhibition of osmotic water flow by general anesthetics to toad urinary bladder. 18 13

Antidiuretic hormone (ADH) administration to a polyuric Miniature Poodle did not alter diuresis. Plasma ADH concentrations were high, and urine osmolality remained low during water deprivation. From these findings, it was concluded that the polyuria was of renal origin. In addition, the glomerular filtration rate was found to be high. Electron microscopic examination of the renal medulla revealed vacuoles containing myelinic figures and fingerprint structures in the cells of the Henle loops, blood vessels, and interstitium, similar to those in lysosomal lipid storage disease. Their absence in collecting duct epithelium indicated that the defect in concentrating ability was due to a disturbance of the counter-current multiplier mechanism rather than to a defect in ADH receptors.
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PMID:Nephrogenic diabetes insipidus in a dog with renal medullary lesions. 50 Apr 24

Inappropriate polyuria leading to hypovolemia and hypotension occurs frequently in severely septic patients. It's etiology was studied in three patients with polyuria and systolic hypotension. Glomerular filtration rate and renal blood flow were measured by the standard renal clearance techniques. Renal blood flow distribution to the outer cortex, inner cortex-outer medulla, and the inner medulla were measured by radioactive xenon. The glomerular filtration rate, renal blood flow, and renal blood flow distribution were normal. Polyuria does not result from a maldistribution of renal blood flow. Antidiuretic hormone did not alter the polyuric syndrome. These data suggest that sepsis produces a blockade at either the distal tubule or the collecting duct, thereby preventing salt and water conservation. This blockade may be due to either a toxin or a toxic metabolic breakdown product of sepsis.
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PMID:Mechanism of inappropriate polyuria in septic patients. 84 54

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

Antidiuretic hormone (ADH) increases toad bladder granular cell apical membrane osmotic water permeability (Pf) by insertion of cytoplasmic vesicles containing water channels into the apical membrane. Termination of ADH stimulation results in endocytosis of water channel-containing membrane. In previous work, we have purified water channel-containing vesicles and demonstrated that they contain 12 major protein bands when analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE). On the basis of vectorial labeling studies of granular cells and purified vesicles, we have proposed previously that vesicle proteins of 55, 53, and 17 kDa are ADH water channel components. In this report, we have purified and analyzed these three proteins using a combination of SDS-PAGE, peptide mapping, amino acid composition, and amino-terminal analyses. The 55- and 53-kDa proteins are distinct protein species possessing a high degree of structural similarity. Both possess a large content of cysteine. The 17-kDa protein appears to be a proteolytic fragment of the 53-kDa protein. None of these three proteins is phosphorylated or contains large amounts of covalently linked carbohydrate. ADH-elicited Pf is inhibited by the organic mercurial reagent fluorescein mercuric acetate (FMA). Exposure of water channel-containing vesicles to FMA labels selectively four vesicle proteins of 92, 55, 53, and 29 kDa while reducing vesicle Pf by 82%. The combination of FMA and 2-mercaptoethanol or exposure to another mercurial reagent, n-ethylmaleimide, does not inhibit vesicle Pf. Together, these data provide additional evidence for the role of the 55- and 53-kDa proteins as components of the ADH water channel. These candidate ADH water channel proteins are distinct from a 28-kDa candidate water channel protein (CHIP 28) isolated recently from human erythrocyte membranes and kidney proximal tubule by Agre and co-workers (Preston, G. M., Carroll, T. P., Guggino, W. B., and Agre, P. (1992) Science 256, 385-387).
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PMID:Purification and partial characterization of candidate antidiuretic hormone water channel proteins of M(r) 55,000 and 53,000 from toad urinary bladder. 142 63

The role of vasopressin and Henle's loop transport in age-related polyuria and decrease in urine osmolality was investigated in female WAG/Rij rats free of kidney disease. In these animals, urine osmolality dropped from 2000 mosmol/kg H2O to 1000-1200 mosmol/kg H2O between 10 and 30 months, and urinary volume increased in proportion. Vasopressin concentration measured in plasma withdrawn from conscious, unrestrained, chronically catheterized rats was not significantly different in 10, 20 and 30-month-old animals (mean values 2.5 +/- 0.7, 2.2 +/- 0.2 and 2.0 +/- 0.3 pg/ml (n = 8), respectively). This suggests an impaired responsiveness of old kidney to antidiuretic hormone. The possible involvement of Henle's loop in this defect was studied by micropuncture. Paired collections of tubular fluid were done in the early distal and late proximal convolutions of the same cortical nephrons. Single nephron filtration rates did not significantly differ with age. Tubular fluid osmolalities in the early distal convolution were 165 +/- 13, 178 +/- 9 and 160 +/- 11 (n = 14) mosmol/kg H2O in 10-, 20- and 30-month-old rats, indicating similar diluting capacity of the cortical thick ascending limb. The amount of sodium transported from lumen to peritubular space by Henle's loop was also unchanged with age as were water, calcium, magnesium and potassium reabsorptions. These data indicate that the age-related decrease in urine osmolality is not related to either a significant reduced vasopressin plasma concentration or an increased single glomerular filtration rate or a reduced transport capacity of Henle's loop of the cortical nephron. Rather they suggest an impaired response to vasopressin of other segments of the nephron that is, the medullary thick ascending limb of Henle's loop and/or the collecting duct.
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PMID:Plasma vasopressin and cortical nephron function in aging rats. 158 12

Antidiuretic hormone (ADH) stimulation of toad urinary bladder granular cells causes simultaneous increases in transepithelial water and H+ permeabilities (PF and PH+, respectively), suggesting that ADH-elicited water channels inserted into granular cell apical membranes might be permeable to both water and H+. We have previously used self-quenching fluorophores entrapped within endocytic vesicles selectively retrieved from water-permeable apical membranes to measure vesicle PF. The membranes of these vesicles possess an extremely high PF such that our measurements provide only minimum estimates of vesicle PF and have limited our ability to quantitate the properties of ADH water channels. We therefore quantitated vesicle PH+ using similar rapid mixing techniques. Vesicle PH+ was 5.1 +/- 0.5 x 10(-3) cm/s. Activation energy of this process was 3.6 +/- 0.6 kcal/mol, indicative of H+ flux through an aqueous channel. The mercurial reagent, para-chloromercuribenzenesulfonate (PCMBS), which inhibits ADH-stimulated transepithelial PF in intact bladders by 50-60%, inhibited vesicle PH+ by 55%. N-Ethylmaleimide and phloretin, which do not alter ADH-stimulated PF, did not affect vesicle PH+. We conclude that membranes containing ADH water channels possess substantial PH+ that likely reflects proton flux through water channels. The apparent high PH+ of the ADH water channel may have important implications for intracellular trafficking of these water channels in ADH-responsive epithelial cells.
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PMID:High proton flux through membranes containing antidiuretic hormone water channels. 169 88

Vasopressin action in the renal collecting duct is believed to be mediated by the cycling of water channels in principal and, possibly, intercalated cells. We used 6-carboxyfluorescein (6-CF) or fluorescein-labeled dextran (FITC-dextran) to determine the location and water permeability of endocytic vesicles from papilla and inner stripe of Brattleboro rats in different states of diuresis. Fifteen minutes after FITC-dextran infusion, fluorescent vesicles were concentrated at the apical pole of principal and intercalated cells. The osmotic water permeability (Pf) of these endosomes was measured by fluorescence quenching. In papillary endosomes, Pf was high (0.04 +/- 0.004 cm/s) when rats were in physiological states of antidiuresis or after treatment with vasopressin, 1-desamino-8-D-arginine vasopressin (DDAVP), or oxytocin; endosomes isolated from these regions of untreated animals had a low Pf. The number of papillary endosomes with high Pf increased with increasing doses of DDAVP. Endosomes from the inner stripe also had a high Pf only after vasopressin treatment. Confocal microscopy of sections of papilla showed that vasopressin significantly increased endocytosis in principal cells but had no effect on intercalated cells. Our data demonstrate that the bulk of fluorescently labeled vesicles from the papilla originate from the apical membrane of principal cells and contain water channels in their limiting membrane only when the rats are in physiological states of antidiuresis. In contrast, the majority of endocytosis in intercalated cells is not involved in water channel recycling.
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PMID:Endocytosis of water channels in rat kidney: cell specificity and correlation with in vivo antidiuresis. 170 69


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