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

The inner medullary collecting duct (IMCD) is widely viewed as a single renal tubule segment with homogeneous properties. However, recent morphological and functional studies have raised the possibility that the initial and terminal parts of the IMCD may differ. To test this possibility further and to localize sites of action of arginine vasopressin (AVP) along the IMCD, we measured osmotic water permeability (Pf) and urea permeability (Purea) in isolated perfused rat IMCDs. In the initial third of the IMCD, 10 nM AVP increased Pf from 16 +/- 8 to 148 +/- 50 micron/s. The terminal two-thirds of the IMCD had a significantly higher basal Pf (70 +/- 12 micron/s), which increased to 186 +/- 25 micron/s with AVP. The initial IMCD had a relatively low basal Purea (3 +/- 1 X 10(-5) cm/s), which did not change with AVP. The terminal IMCD had a significantly higher basal Purea (17 +/- 4 X 10(-5) cm/s), which increased to a very high value (69 +/- 15 X 10(-5) cm/s) with AVP. The results support the premise that (from the point of view of vasopressin effects on water and urea transport) there are two functionally distinct parts of the inner medullary collecting duct: an initial part that resembles the cortical or outer medullary portions of the mammalian collecting duct and a terminal part that resembles the toad urinary bladder. The significance of these findings for the urinary concentrating mechanism is discussed.
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PMID:Vasopressin effects on urea and H2O transport in inner medullary collecting duct subsegments. 368 38

Several factors interact to maintain precise control of electrolyte transport in the mammalian cortical collecting duct. We have studied the effects of deoxycorticosterone, arginine vasopressin, and bradykinin on net transepithelial sodium and potassium transport in isolated, perfused rat cortical collecting ducts. Chronic administration of deoxycorticosterone to rats increased both sodium absorption and potassium secretion above very low basal levels. Consequently, deoxycorticosterone-treated rats were used for all remaining studies. Arginine vasopressin (10(-10) M in the bath) caused a sustained fourfold increase in net sodium absorption and a sustained threefold increase in net potassium secretion. Bradykinin (10(-9) M in the bath) caused a reversible 40-50% inhibition of net sodium absorption without affecting net potassium transport or the transepithelial potential difference. In the perfusate, up to 10(-6) M bradykinin had no effect. We conclude: As in rabbits, chronic deoxycorticosterone administration to rats increases sodium absorption and potassium secretion in cortical collecting ducts perfused in vitro. Arginine vasopressin causes a reversible increase in net potassium secretion and net sodium absorption. Bradykinin in the peritubular bathing solution reversibly inhibits net sodium absorption, possibly by affecting an electroneutral sodium transport pathway.
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PMID:Control of sodium and potassium transport in the cortical collecting duct of the rat. Effects of bradykinin, vasopressin, and deoxycorticosterone. 401 71

We suggested previously, on the basis of indirect evidence, that in two strains of mice with nephrogenic defects of urinary concentration the deficiency arose from an inadequate rise in water permeability of the collecting duct system. In this study we tested the question further by assuming that the frequency of intramembranous particle (IMP) clusters seen by freeze-fracture can be used as a morphological marker of vasopressin-induced water permeability. Three genotypes of mice were studied: 1) DI +/+ Severe, with florid, vasopressin-resistant diabetes insipidus; 2) DI +/+ Nonsevere, with an intermediate deficiency of urinary concentration; and 3) normal, VII +/+ mice. In addition, we examined a group of DI +/+ Severe mice that had been injected with exogenous 1-desamino-8-D-arginine vasopressin (DDAVP) subcutaneously for 3 days. Since the results in this group did not differ from those in untreated DI +/+ Severe mice, all data for this genotype were combined. IMP clusters within luminal membranes of inner medullary collecting duct principal cells were quantified by freeze-fracture electron microscopy. Urinary osmolality and percentage of cells showing clusters were, respectively: 203 +/- 43 mosmol/kg H2O and 0% in DI +/+ Severe mice; 1,133 +/- 86 and 33 +/- 4 in DI +/+ Nonsevere mice; and 2,234 +/- 190 and 52 +/- 5 in VII +/+ animals. With the exception of one animal, there was no overlap of the data, which were significantly different from one another for each variable. We conclude that in DI +/+ Severe mice, both endogenous and exogenous vasopressin are unable to increase the water permeability of medullary collecting ducts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Lack of intramembranous particle clusters in collecting ducts of mice with nephrogenic diabetes insipidus. 405 Oct 7

The present study was undertaken to investigate the cyclic AMP system in the isolated inner medullary collecting tubule (IMCT) of hypokalemic (HK) rats. In situ incubation of IMCT with 10(-7) M arginine vasopressin (AVP) at 300 mOsm/kg H2O in control normokalemic rats increased cyclic AMP content (fmoles/mm) from 5.68 +/- 1.41 to 30.3 +/- 5.31 (P less than 0.001). In HK rats the increase in cyclic AMP was blunted from 7.18 +/- 2.0 to 14.78 +/- 3.14 fmoles/mm (P less than 0.05 compared to controls). No such blunting was observed in the outer medullary collecting duct of hypokalemic rats, but was seen in the IMCT when studied at 800 (P less than 0.05), 1200 (P less than 0.01), and 2000 mOsm/kg H2O (P less than 0.05). The increase in cyclic AMP was also blunted in IMCT of HK rats not allowed to become polyuric or polydipsic by pair-watering studied at 300, 800, and 1200 mOsm/kg H2O. To define the process responsible for the failure to normally increase cyclic AMP in HK, adenylate cyclase activity (AC) was determined at 800 mOsm/kg H2O. While basal AC was not different, the response to all concentrations of AVP between 10(-10) and 10(-6) M was markedly depressed in tubules from HK rats. In contrast AC response to 10(-2) M NaF was not different in IMCT of normokalemic and HK rats. While the abnormal cyclic AMP content with AVP could be explained by abnormal generation, a contribution of increased metabolism was also sought.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The cyclic AMP system in the inner medullary collecting duct of the potassium-depleted rat. 609 65

Hyperosmolality occurs when there are defects in the two major homeostatic mechanisms required for water balance-thirst and arginine vasopressin (AVP) release. In this situation hypotonic fluids are lost in substantial quantities causing depletion of both intracellular and extracellular fluid compartments. Patients with essential hypernatremia have defective osmotically stimulated AVP release and thirst but may have intact mechanisms for AVP release following hypovolemia. Hyperosmolality can also be seen in circumstances in which impermeable solutes are present in excessive quantities in extracellular fluid. Under these conditions there is cellular dehydration and the serum sodium may actually be reduced by water drawn out of cells along an osmotic gradient. Hyposmolality and hyponatremia may be seen in a variety of clinical conditions. Salt depletion, states in which edema occurs and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) may all produce severe dilution of body fluids resulting in serious neurologic disturbances. The differential diagnosis of these states is greatly facilitated by careful clinical assessment of extracellular fluid volume and by determination of urine sodium concentration. Treatment of the hyposmolar syndromes is contingent on the pathophysiology of the underlying disorder; hyponatremia due to salt depletion is treated with infusions of isotonic saline whereas mild hyponatremia in cirrhosis and ascites is best treated with water restriction. Severe symptomatic hyponatremia due to SIADH is treated with hypertonic saline therapy, sometimes in association with intravenous administration of furosemide. Less severe, chronic cases may be treated with dichlormethyltetracycline which blocks the action of AVP on the collecting duct.
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PMID:The clinical physiology of water metabolism. Part III: The water depletion (hyperosmolar) and water excess (hyposmolar) syndromes. 624 83

A homogeneous population of single cells from the thick ascending limb of Henle's loop (TALH) has been isolated from the rabbit kidney medulla. A total medullary cell suspension was prepared by a series of collagenase, hyaluronidase, and trypsin digestions and separated on a Ficoll gradient (2.6-30.7% wt/wt). Morphologically, the cells isolated from the TALH were homogeneous and showed polarity within their plasma membrane structure, with a few blunt microvilli on their apical surface and deep infoldings of the basal-lateral membrane. Biochemically, the TALH cells were highly enriched in calcitonin-sensitive adenylate cyclase and Na, K-ATPase. Alkaline phosphatase and arginine vasopressin-sensitive adenylate cyclase, highly concentrated in proximal tubule and collecting duct, were present only in low concentrations in the TALH cells. Additionally, furosemide, a diuretic inhibiting sodium chloride transport in the TALH in vivo, inhibited oxygen consumption of the TALH cells in a dose-dependent manner. The TALH cells were viable, as judged by morphological appearance, trypan blue exclusion, the response of oxygen consumption to 2,4-dinitrophenol, succinate and ouabain, and the cellular Na, K and ATP levels.
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PMID:Separation of renal medullary cells: isolation of cells from the thick ascending limb of Henle's loop. 625 27

Among other defects in water metabolism, adrenal insufficiency is associated with an inability to concentrate urine maximally in both man and experimental animals. Recent studies in the rabbit cortical collecting tubule have suggested indirectly that this defect may result from impaired cyclic AMP (cAMP) formation in response to antidiuretic hormone stimulation. In the present study, we examined key elements of arginine vasopressin (AVP)-dependent cAMP metabolism in the papillary collecting duct (PCD), microdissected from 8-d adrenalectomized (ADX) and sham-operated control rats. AVP-sensitive adenylate cyclase (ADC) activity in PCD did not differ between control and ADX rats. cAMP-phosphodiesterase activity (cAMP-PDIE), measured at 10(-6) M cAMP substrate concentration, was significantly higher (delta + 31.6%) in PCD of ADX rats compared with controls. Incubation of intact PCD from ADX rats with AVP resulted in an accumulation of cAMP (delta - 48.5%) significantly lower than observed in control PCD. Chronic administration of dexamethasone reduced cAMP-PDIE activity in PCD of ADX rats to levels close to or below those observed in control rat PCD, and also resulted in a restoration of AVP-stimulated cAMP accumulation to levels approaching control values. Results indicate that the impaired maximal urinary concentrating ability associated with adrenal insufficiency may be due, at least in part, to a reduced accumulation of cAMP in response to AVP in the PCD. This decreased cAMP accumulation results from increased cAMP-PDIE activity in the PCD of ADX rats and can be corrected by administration of glucocorticoid.
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PMID:Concentrating defect in the adrenalectomized rat. Abnormal vasopressin-sensitive cyclic adenosine monophosphate metabolism in the papillary collecting duct. 630 13

Exogenous endothelin-1 (ET-1) inhibits arginine vasopressin (AVP)-induced cAMP accumulation in the inner medullary collecting duct (IMCD). Because ET-1 is produced by and binds to specific receptors on the IMCD, the possibility exists that ET-1 is an autocrine regulator of AVP action in this nephron segment. To test this hypothesis, rat IMCD cells were grown on semipermeable membranes in the presence of rabbit anti-ET-1 antiserum or nonimmune rabbit serum (NRS). AVP (10(-9) M) caused a 2.5-fold greater accumulation of cAMP in confluent IMCD monolayers preincubated in ET-1 antiserum in comparison with NRS. ET-1 (10(-8) M) inhibited the AVP-induced rise in cAMP by 65% in cells preincubated in ET-1 antiserum but had no effect in NRS-treated cells. Finally, [125I]-ET-1 (30 pM) binding was increased sixfold in IMCD preincubated in anti-ET-1 antiserum. These data indicate that ET-1 causes tonic autocrine inhibition of AVP responsiveness in the IMCD.
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PMID:Autocrine role of endothelin in rat inner medullary collecting duct: inhibition of AVP-induced cAMP accumulation. 750 36

Several membranes of the kidney are highly water permeable, thereby enabling this organ to retain large quantities of water. Recently, the molecular identification of water channels responsible for this high water permeability has finally been accomplished. At present, four distinct renal water channels have been identified, all members of the family of major intrinsic proteins. Aquaporin 1 (AQP1), aquaporin 2 (AQP2) and the mercury-insensitive water channel (MIWC) are water-selective channel proteins, whereas the fourth, referred to as aquaporin 3 (AQP3), permits transport of urea and glycerol as well. Furthermore, a putative renal water channel (WCH3) has been found. AQP1 is expressed in apical and basolateral membranes of proximal tubules and descending limbs of Henle, AQP2 predominantly in apical membranes of principal and inner medullary collecting duct cells and AQP3 in basolateral membranes of kidney collecting duct cells. MIWC is expressed in the inner medulla of the kidney and has been suggested to be localised in the vasa recta. The human genes encoding AQP1 and AQP2 have been cloned, permitting deduction of their amino acid sequence, prediction of their two-dimensional structure by hydropathy analysis, speculations on their way of functioning and DNA analysis in patients with diseases possibly caused by mutant aquaporins. Mutations in the AQP1 gene were recently detected in clinically normal individuals, a finding which contradicts the presumed vital importance of this protein. Mutations in the AQP2 gene were shown to cause autosomal recessive nephrogenic diabetes insipidus. The renal unresponsiveness to arginine vasopressin, which characterises this disease, is in accordance with the assumption that AQP2 is the effector protein of the renal vasopressin pathway.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Discovery of aquaporins: a breakthrough in research on renal water transport. 754 Aug 50

Previously, we have shown in porcine inner medullary collecting duct (IMCD) cells that endothelin (ET), probably in an autocrine fashion, suppresses arginine vasopressin (AVP)-induced synthesis of cAMP and thereby, may modify the action of AVP on IMCD fluid transport. In the present study we investigated the effects of various stimuli including extracellular tonicity on ET synthesis in porcine IMCD cells in culture. IMCD cells produced ET in a saturationlike time-dependent manner over a period of 24 h. Neither AVP (10(-7) mol/L), bradykinin (10(-7) mol/L), nor atrial natriuretic peptide (10(-7) mol/L) affected basal ET synthesis of IMCD cells at extracellular isotonicity (323 mOsm/kg H2O). The calcium ionophore A23187 (10(-7) mol/L) increased ET production by 38% within 2 h (P < .05). Preincubation for 48 h with increased osmolality in the incubation media from 323 to 600 mOsm/kg H2O by raising the concentrations of 1) NaCl (n = 6), 2) urea (n = 6), or 3) NaCl+urea (n = 6) increased ET synthesis from a control value of 225 +/- 25 pg/mg cell protein/2 h in isotonic medium to 1) 555 +/- 13 pg/mg cell protein/2 h (P < .01), 2) 354 +/- 18 pg/mg cell protein/2 h (P < .05), and 3) 448 +/- 22 pg/mg cell protein/2 h (P < .05), respectively, in hypertonic media. These data suggest that increases in papillary osmolality are associated with enhanced ET synthesis possibly involving a calcium-dependent process and attenuating AVP-dependent fluid absorption in a short-loop feedback fashion.
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PMID:Endothelin synthesis by porcine inner medullary collecting duct cells. Effects of hormonal and osmotic stimuli. 754 2


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