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)

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

The permeability of the tight junctions (zonulae occludentes) was evaluated along the entire length of the collecting duct of the rat using a lanthanum tracer technique. Nine rats with hereditary hypothalamic diabetes insipidus were studied using standard micropuncture and clearance techniques. Glomerular filtration rate (GFR) estimated from inulin clearance, urine and plasma osmolality (U/Posm) and urine flow rate (V) were determined in eight of nine animals. During either sustained diuresis (five animals) or vasopressin-induced antidiuresis (four animals), individual surface convolutions of distal convoluted tubules or early cortical collecting ducts were preserved for ultrastructural examination by intraluminal microperfusion with a glutaraldehyde-formaldehyde fixative followed by a second microperfusion with a lanthanum tracer. Mean GFR during diuresis was 6.31 plus or minus se 0.63 ml/min/kg of body wt and v=797 plus or minus se 108 mul/min/kg or 13.6 plus or minus se 2.2% of the filtered load of water. After administration of exogenous vasopressin, V fell to 311 plus or minus 157 mul/min/kg or 5.2 plus or minus se 3.8% of the filtered load of water and U/Posm rose from 0.658 plus or minus se 0.043 to 2.124 plus or minus 0.454. Tight junctions of cortical and outer medullary segments of the collecting duct resisted lanthanum penetration. Tight junctions of the inner medullary and papillary segments of the collecting duct were freely permeable to lanthanum suggesting the presence of a paracellular shunt pathway for solute and water movement. The results were independent of the presence or absence of vasopressin. Physiological studies have previously demonstrated that cortical and outer medullary segments of the collecting duct have a low urea permeability while inner medullary and papillary segments of the collecting duct have a relatively high urea permeability. The possibility is suggested that urea movement across the inner medullary and papillary segments of the collecting duct may occur, at least in part, via a paracellular pathway formed by the nonoccluding tight junction and the lateral intercellular space.
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PMID:Lanthanum permeability of tight junctions along the collecting duct of the rat. 112 64

Experiments were performed in anesthetized rats to examine the possibility that endothelin (ET) modifies renal epithelial function in addition to its well-established hemodynamic actions. Infusion of ET-3 at rates between 34 and 178 ng.kg-1.min-1 was in many cases followed by a rise in urine flow and a persistent decrease in urine osmolality, whereas glomerular filtration rate (GFR) did not significantly change. The extent of ET-induced diuresis was dependent on the response of GFR: in rats in which ET-3 infusion caused a marked reduction of GFR (greater than 70%) ET-induced diuresis was not seen, even though urine osmolality still fell significantly. From animal to animal, ET-induced changes of urine flow or GFR did not correlate significantly with the rate of ET-3 infusion. ET-1, another ET isopeptide, also produced water diuresis when administered in GFR-neutral doses. Urinary excretion of total solutes and of sodium was not significantly altered by ET-3. Infusion of vasopressin blunted the diuretic effect of ET-3, whereas ET-3-induced water diuresis was not measurably altered by chronic or acute treatment with a converting enzyme inhibitor or by acute inhibition of prostaglandin synthesis. Induction of water diuresis was not secondary to an inhibition of vasopressin secretion since it could be demonstrated in homozygous Brattleboro rats in which antidiuresis was produced by the infusion of vasopressin at a rate of 200 microU.kg-1.min-1. These data suggest that ET may be an inhibitory modulator of the hydrosmotic action of vasopressin at the level of the renal collecting duct.
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PMID:Induction of water diuresis by endothelin in rats. 141 80

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

The present in vitro microperfusion study examined whether chlorpropamide (CPM) has a direct effect on hydraulic conductivity (Lp x 10(-6) cm/atm.sec) and 14C-urea permeability (Pu x 10(-5) cm/sec) in the middle and distal inner medullary collecting duct (IMCD) obtained from acutely water-loaded Wistar rats and rats homozygous for diabetes insipidus (DI). CPM (10(-4) M) added to the bath fluid increased the Lp in the water-loaded Wistar rats from -0.05 +/- 0.13 to 6.25 +/- 0.74 (p less than 0.01) and in the DI rats from 0.05 +/- 0.01 to 5.95 +/- 0.84 (p less than 0.01), but had no effect when it was added to the perfusate. CPM stimulated Lp in a dose-dependent manner with the threshold effect at 10(-6) M. However, the addition of CPM (10(-4) M) to submaximal concentration of VP in the bath fluid did not increase the Lp. Furthermore, CPM was unable to block the inhibitory action of PGE2 on the vasopressin (VP)-stimulated Lp. On the contrary, PGE2 blocked the CPM-stimulated Lp. CPM (10(-4) M) in the peritubular fluid was able to cause a significant rise of the Pu from 13.5 +/- 0.8 to 17.3 +/- 1.0 reversibly, which represented 16% of maximum stimulated effect produced by 50 microU/ml of VP. Thus, pharmacological doses of CPM added to the peritubular side have a direct effect on terminal IMCD increasing water and urea permeability in the absence of VP, but this drug does not potentiate the VP-stimulated water transport in the IMCD. Our results were unable to confirm the hypothesis that CPM potentiates the VP-antidiuresis by the inhibition of PGE2 action in the rat IMCD.
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PMID:Effect of chlorpropamide on water and urea transport in the inner medullary collecting duct. 200 36

The renal response to changes in hydration includes variation in intracellular sorbitol, a major inner medullary osmolyte. To examine the mechanism for changes in net sorbitol production, we measured activities of enzymes regulating sorbitol production (aldose reductase) and degradation (sorbitol dehydrogenase) in untreated, water diuretic, and antidiuretic (water restriction and/or vasopressin administration) rats. Collecting duct segments dissected from collagenase-treated kidneys of Sprague-Dawley rats were divided into outer medullary and three distinct inner medullary regions. Aldose reductase activity increased during antidiuresis and decreased during diuresis. In contrast, sorbitol dehydrogenase activity was very low during antidiuresis and increased during diuresis. These changes in enzyme activity were found after 3 days, but not after 1 day, of water diuresis/antidiuresis. Enzyme activity changed only in the deepest 50% of the inner medullary collecting duct. Thus, there is coordinated regulation of aldose reductase and sorbitol dehydrogenase activities so that (a) during water diuresis, aldose reductase activity decreases while sorbitol dehydrogenase activity increases; and (b) during antidiuresis (water restriction and/or vasopressin administration), aldose reductase activity increases while sorbitol dehydrogenase activity remains low. We conclude that long-term osmoregulation in response to physiologic stimuli involves both aldose reductase and sorbitol dehydrogenase activities in rat terminal inner medullary collecting duct segments.
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PMID:Coordinated response of renal medullary enzymes regulating net sorbitol production in diuresis and antidiuresis. 212 8

Fourteen subjects with persistent azotemia and normal glomerular filtration rate were studied by renal clearances and hormonal determinations to establish the nephron site of altered urea transport and the mechanism(s) responsible for their azotemia. During constant alimentary protein, urea nitrogen appearance was normal and urea clearance was much lower than in 10 age-matched control subjects (23.3 +/- 2.1 ml/min and 49.6 +/- 2.6 ml/min per 1.73 m2, P less than 0.001). Inulin and para-aminohippurate clearances, blood volume and plasma concentration of antidiuretic hormone were within normal limits. During maximal antidiuresis, in spite of greater urea filtered load, the urinary excretion of urea was less, and both the maximum urinary osmolality and the free-water reabsorption relative to osmolar clearance per unit of GFR were greater than in control subjects. After sustained water diuresis, the plasma urea concentration markedly decreased to near normal levels in azotemic subjects. The basal urinary excretion of prostaglandins E2 was significantly reduced in azotemic subjects and was directly correlated with fractional urea clearance (r = 0.857, P less than 0.001). An additional group of control subjects (N = 8) showed a marked reduction of fractional clearance of urea after inhibition of prostaglandin synthesis (P less than 0.01). These data suggest that azotemia is due to increased tubular reabsorption of urea in the distal part of nephron, presumably because of increased back diffusion in the papillary collecting duct, accounting for the enhanced maximum urinary osmolality and free-water reabsorption. Renal prostaglandin E2 may participate in the pathogenesis of azotemia by altering recycling of urea in the medulla.
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PMID:Renal handling of urea in subjects with persistent azotemia and normal renal function. 332

It has been hypothesized that urea from the final urine is recycled into the renal papilla through the pelvic epithelium. To test this hypothesis, samples of urine were collected by micropuncture proximally and distally through the intact, contracting ureter of the anesthetized rat. In 12 rats, in which urine flow was 5.89 +/- 0.67 microliter/min (a moderate antidiuresis), the ratio of proximal-to-distal urea concentration, corrected for water movement, was 0.93 +/- 0.03 (P less than 0.01 compared with unity), indicating that approximately 7% of urea in the urine emerging from the terminal collecting duct was reabsorbed by the time it reached the distal ureter. To assess the possible contribution of urea reabsorption by the ureter, the ureter was cannulated proximally and distally and perfused with urine of known composition at 6.26 +/- 0.10 microliter/min. In nine rats, the ratio of urea concentration in the perfusate collected from the distal end of the ureter to that in the perfusate entering the proximal end was 0.93 +/- 0.02 (P less than 0.01 compared with unity), indicating 7% reabsorption. Movement of solute across the ureteral epithelium was not restricted to urea. Potassium and creatinine were also reabsorbed [3.4 +/- 0.9 (P less than 0.01) and 3.5 +/- 1.2% (P less than 0.05), respectively], whereas sodium was secreted [9.2 +/- 2.3% (P less than 0.01)].(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Urea flux in the ureter. 340 82

The microcatheterization technique was used to examine electrolyte transport in the medullary collecting duct of two groups of anesthetized rats during water diuresis and during a second experimental phase with 1-desamino-8-D-arginine vasopressin (dDAVP) administration or continued water diuresis. Potassium reabsorption of 53-61% of the delivered load was consistently observed in the medullary collecting duct during water diuresis. During dDAVP administration, urinary potassium excretion doubled, and there was no net potassium transport (reabsorption or secretion) in the medullary collecting duct. The change in potassium transport in medullary collecting duct from water diuresis to antidiuresis (dDAVP) was sufficient to account for the increase in urinary potassium excretion. Changes in flow rate, luminal sodium concentration, or collecting duct sodium reabsorption could not account for the changes in potassium transport in the collecting duct during dDAVP. The results are interpreted as indicating that dDAVP stimulates potassium entry (secretion) into the medullary collecting duct, probably by a direct effect. This action of antidiuretic hormone appears to be important in maintaining potassium homeostasis during changing water balance.
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PMID:Effect of vasopressin analogue (dDAVP) on potassium transport in medullary collecting duct. 359 61

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


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