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

The ultrastructure of the distal nephron, the collecting duct and the Wolffian duct was studied in a South American caecilian, Typhlonectes compressicaudus (Amphibia, Gymnophiona) by transmission and scanning electron microscopy (TEM, SEM). The distal tubule (DT) is made up of one type of cell that has a well-developed membrane labyrinth established both by interdigitating processes and by interlocking ramifications. The processes contain large mitochondria, the ramifications do not. The tight junction is shallow and elongated by a meandering course. The connecting tubule (CNT) is composed of CNT cells proper and intercalated cells, both of which are cuboidal in shape. The CNT cells are characterized by many lateral interlocking folds. The intercalated cells have a dark cytoplasm densely filled with mitochondria. Their apical cell membrane is typically amplified by microplicae beneath which a layer of globular particles (studs) is found. The collecting duct (CD) is composed of principal cells and intercalated cells, again both cuboidal in shape. The CD epithelium is characterized by dilated intercellular spaces, which are often filled with lateral microfolds projecting from adjacent principal cells. The apical membrane is covered by a prominent glycocalyx. The intercalated cells in the CD are similar to those in the CNT. The Wolffian duct (WD) has a tall pseudostratified epithelium established by WD cells proper, intercalated cells and basal cells. The WD cells contain irregular-shaped dense granules located beneath the apical cell membrane. The intercalated cells of the WD have a dark cytoplasm with many mitochondria; their nuclei display a dense chromatin pattern.
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PMID:Ultrastructure of the kidney of a South American caecilian, Typhlonectes compressicaudus (Amphibia, Gymnophiona). II. Distal tubule, connecting tubule, collecting duct and Wolffian duct. 339 58

1. In order to explore the involvement of endogenous prostaglandin E2 (PGE2) in the urine concentration defect after ureteral occlusion, PGE2 production by isolated collecting ducts in vitro and effects of indomethacin on urine osmolality in vivo were examined. 2. Twenty-four hours ureter obstruction caused increased PGE2 production by the medullary collecting ducts, which was maintained at a high level on the day after release of obstruction (0.8 +/- 0.2 pg/mm normal, 8.1 +/- 0.9 pg/mm 24 h obstruction, and 6.6 +/- 1.0 pg/mm post-obstruction, mean +/- SEM). An enhanced PGE2 production was also observed for papillary collecting duct on the day after release of 24 h ureteral occlusion (3.9 +/- 0.5 pg/mm normal and 7.7 +/- 1.2 pg/mm post-obstruction). 3. Administration of indomethacin to the unilateral post-obstructive rats slightly raised the urine osmolality of the post-obstructed kidney (from 339 +/- 17 to 390 +/- 22 mosmol/kg H2O), while it had a greater effect on the contralateral intact kidney (from 1569 +/- 138 to 2567 +/- 198 mosmol/kg H2O). 4. Our data may indicate that the urine concentration defect after 24 h ureteral occlusion is ascribable mainly to a mechanism other than increased endogenous PGE2.
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PMID:Tubular prostaglandin E2 production and its role in urinary hypotonicity after release of ureteral occlusion in the rat. 347 70

The element concentrations in various intra- and extracellular compartments of the tip of the rat renal papilla were determined during antidiuresis using electron microprobe analysis. Urinary concentrations (means +/- SEM) were: urea, 1509 +/- 116; potassium, 268 +/- 32; sodium, 62 +/- 19 mmoles X 1(-1); and osmolality, 2548 +/- 141 mOsm X kg-1. Electrolyte concentrations in the interstitial space were: sodium, 437 +/- 19; chloride, 438 +/- 20; and potassium, 35 +/- 2 mmoles X kg-1 wet wt. The vasa recta plasma exhibited almost identical element concentrations. The values in the papillary collecting duct cells were: sodium, 28 +/- 1; chloride, 76 +/- 3; potassium, 135 +/- 3; and phosphorus, 316 +/- 7 mmoles X kg-1 wet wt. Similar concentrations were observed in the papillary epithelial cells. In interstitial cells potassium and phosphorus concentrations were virtually identical to those of the collecting duct cells, whereas sodium and chloride concentrations were higher by about 30 mmoles X kg-1 wet wt. The element composition of the various papillary cells is, thus, not substantially different from that of proximal tubular cells. This finding demonstrates that cellular accumulation of electrolytes is not the regulatory mechanism by which papillary cells adapt osmotically to their high environmental osmolality and sodium chloride concentration.
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PMID:Intra- and extracellular element concentrations of rat renal papilla in antidiuresis. 672 35

The effect of prostaglandin on diffusional water permeability has been studied in collecting ducts in an isolated rat papilla. PGE2 increased water permeability. The effect was significant at a concentration of 10(-8) mol 1(-1) and was maximal with a concentration of 10(-6) mol 1(-1). The maximal increment of 0.94 +/- 0.10 (SEM) micron s-1 was approximately half that produced by maximal stimulation with antidiuretic hormone (2.18 +/- 0.12 micron s-1). A concentration of 10(-8) mol 1(-1) produced an increase in basal water permeability and 24 mu unit ml-1 ADH, which without PGE2 present gave a similar increase, had no incremental effect. ADH 100 mu unit ml-1 increased permeability to a value similar to that observed in the absence of PGE2. Thus PGE2 and ADH both increase water permeability but the increments are not additive. Indomethacin in a concentration that inhibited prostaglandin production altered the response of the collecting duct to ADH. The dose response curve was shifted to the left and the maximal increase in water permeability and the lowest dose at which a response occurred took place at concentrations less than 1/2 those required in its absence. Prostaglandins influence the action of ADH and it is likely that in life they regulate and modulate the change in water permeability induced by anti-diuretic hormone.
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PMID:The effect of prostaglandin E2 and ADH on diffusional water permeability in collecting duct of an isolated rat papilla. 694 74

Transmission electron micrographs of the mesonephric nephron in 18 day rabbit embryos reveal major cytological structures reappearing in the nephron of the definitive rabbit kidney. The initial segment of the proximal tubule resembles (despite quite different cell proportions) the cell picture of the metanephric S2-segment. The changes occurring at the end of the terminal proximal segment, the decrease in cell size, flattening of the nuclei, shortening of the brush border and reduction of Golgi profiles and endocytotic organelles largely parallel those between S2 and S3. The type of increased basolateral cell face of the proximal and distal tubule cells shows only quantitative differences to their metanephric counterparts. The distal tubule, which cannot be further subdivided (except the macula densa-region) exhibits varying degrees of cell interdigitations with vertically arranged and partially arching lateral ridges. This tubule matches closely the metanephric medullary straight part of the distal tubule, so that the sequence of the first mesonephric nephron segments is similar to the metanephric ones with the exception that the thin limb of Henle is absent. The large macula densa-region is characterized by its cell height and distended infranuclear spaces. The principal cells of the collecting tubule, with a few basal infoldings and intense short lateral interlockings resemble metanephric cells of the outer medullary collecting duct. The mitochondria-rich intercalated cells occur in dark and light contrasting forms and are more frequent than was evident from our SEM-study. The homogenous cell population of the Wolffian duct is characterized by large glycogen deposits and comparatively smooth cell faces.
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PMID:The mature mesonephric nephron of the rabbit embryo. II. TEM-studies. 724 60

We examined renal sodium handling in rats with Hymann nephritis (HEN), an immunologically mediated model of nephrotic syndrome. Rats were studied 9-14 days following i.p. injection of anti-Fx1A antiserum. We previously demonstrated that HEN had a blunted volume expansion natriuresis (2% body weight isotonic saline infused over 5 min), excreting sodium at only half the rate of normal controls (CTL) despite similar increase in plasma atrial natriuretic peptide (ANP) concentration. Urinary excretion of cGMP accumulation by isolate glomeruli and inner medullary collecting duct (IMCD) cells in response to increasing concentration of ANP, and RNP (also called urodilatin). Results (fmol/mg prot/10 min) are means +/- SEM: [table: see text]. Basal accumulation of cGMP was not different among the groups, HEN rats hd reduced cGMP accumulation in response to ANP, and RNP. In binding studies using 125I-ANP, no difference in either density or affinity was found between CTL and HEN rats. Thus, there is a renal resistance to ANP in rats with HEN, which can be extended to other agents acting through the cGMP pathway. This resistance is not due to impaired binding of ANP, but to impaired accumulation of cGMP in responsive tissues, reflecting perhaps increased cGMP catabolism by phosphodiesterase. Such an observation may account for the altered sodium handling in nephrotic rats.
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PMID:[Resistance to the action of atrial natriuretic peptide and urodilatin in Heymann nephritis in vitro]. 775 73

We examined the actions of potentially natriuretic autacoids in the isolated perfused cortical collecting duct (CCD) dissected from inbred Dahl (Rapp strain) salt-sensitive rats (SS). Atrial natriuretic peptide (ANP, 10 nM), bradykinin (BK, 10 nM), and clonidine (1 microM) were studied to determine their effects on the lumen-to-bath flux of 22Na+ (J1-->b, pmol min-1 mm-1), hydraulic conductivity (Pf, micron/s), and transepithelial voltage (VT, mV). ANP and BK have been shown by others to significantly reduce net Na+ reabsorption and hydraulic conductivity in the Sprague-Dawley (SD) rat CCD, but previous results from our laboratory showed no ANP or BK effect in the SD CCD. In the present study, we were also unable to observe any effect of either ANP or BK in the SS rat CCD. However, in the presence of AVP, clonidine (a partial alpha 2-adrenergic receptor agonist) significantly reduced J1-->b and Pf from 139 +/- 6 (SEM) to 88 +/- 7 and from 959 +/- 176 to 490 +/- 73, respectively. In addition, clonidine significantly depolarized VT from -14.5 +/- 2.8 to -11.2 +/- 1.8. However, unlike its effects in the SD rat CCD, yohimbine (300 nM, an alpha 2-adrenergic receptor antagonist) did not significantly reverse the effects of clonidine on J1-->b, Pf or VT in the SS rat CCD.
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PMID:Clonidine, but not bradykinin or ANP, inhibits Na+ and water transport in Dahl SS rat CCD. 835 63

Confluent M-1 cells show electrogenic Na+ absorption and possess an amiloride-sensitive Na(+)-conductance (Korbmacher et al., J. Gen. Physiol. 102:761-793, 1993). In the present study, we further characterized this conductance and identified the underlying single channels using conventional patch clamp technique. Moreover, we isolated poly(A)+ RNA from M-1 cells to express the channels in Xenopus laevis oocytes, and to check for the presence of transcripts related to the epithelial Na+ channel recently cloned from rat colon (Canessa et al., Nature 361:467-470, 1993). Patch clamp experiments were performed in 6-13-day-old confluent M-1 cells at 37 degrees C. In whole-cell experiments application of 10(-5) M amiloride caused a hyperpolarization of 24.9, SEM +/- 2.2 mV (n = 35) and a reduction of the inward current by 107 +/- 10 pA (n = 51) at a holding potential of -60 mV. Complete removal of bath Na+ had similar effects, indicating that the amiloride-sensitive component of the inward current is a Na+ current. The effect of amiloride was concentration-dependent with half-inhibition at 0.22 microM. The Na+ current saturated with increasing extracellular Na+ concentrations with an apparent Km of 24 mM. Na+ replacement for Li+ demonstrated a higher apical membrane conductance for Li+ than for Na+. In excised inside-out (i/o) or outside-out (o/o) patches from the apical membrane, we observed single-channels which showed slow kinetics and were reversibly inhibited by amiloride. Their average conductance for Na+ was 6.8 +/- 0.5 pS (n = 15) and for Li+ 11.2 +/- 1.0 pS (n = 14). They had no measurable conductance for K+. In o/o patches, channel activity was slightly voltage dependent with an open probability (NPo) of 0.46 +/- 0.14 and 0.16 +/- 0.05 at a holding potential of -100 and 0 mV, respectively (n = 8, P < 0.05). Using the two-microelectrode voltage-clamp technique, we assayed defolliculated stage V-VI Xenopus oocytes for an amiloride-sensitive inward current 1-6 days after injection with H2O or with 20-50 ng of M-1 poly(A)+ RNA. In poly(A)+ RNA-injected oocytes held at -60 or -100 mV application of amiloride (2 microM) reduced the Na-inward current by 25.5 +/- 4.6 nA (n = 25) while it had no effect in H2O-injected oocytes (n = 19). Northern blot analysis of M-1 poly(A+) RNA revealed the presence of transcripts related to the three known subunits of the rat colon Na+ channel (Canessa et al., Nature 367:463-467, 1994). We conclude that the channel in M-1 cells is closely related to the amiloride-sensitive epithelial Na+ channel in the rat colon and that the M-1 cell line provides a useful tool to investigate the biophysical and molecular properties of the corresponding channel in the cortical collecting duct.
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PMID:Amiloride-sensitive sodium channels in confluent M-1 mouse cortical collecting duct cells. 860 62

Water transport across the mammalian collecting tubule is regulated by vasopressin-dependent aquaporin-2 insertion into and retrieval from the apical cell membrane. To establish a cell line that properly expresses aquaporin-2 and its hormone-dependent shuttling, Madin-Darby canine kidney cells were stably transfected with an aquaporin-2 expression construct. Cells of a representative clone (wild-type 10 [WT-10]) were grown on semipermeable supports, and transcellular osmotic water permeability (Pf; in microm/s +/- SEM) was measured. The basal Pf of WT-10 cells, which was lowered with indomethacin, increased from 10.6 +/- 0.8 to 35.7 +/- 1.2 upon incubation with 1-desamino-8-D-arginine vasopressin (dDAVP). This increase coincided with the translocation of aquaporin-2 from an intracellular compartment to the apical membrane. The Pf of untransfected cells (6.5 +/- 0.8) was unchanged by dDAVP. Kinetic studies with WT-10 cells revealed that maximal Pf was obtained within 30 min after dDAVP addition, which remained elevated for at least 90 min. Intracellular cAMP levels peaked within 5 min after dDAVP admission and decreased to basal levels within 45 min. After preincubation with dDAVP, the Pf decreased within 15 min after dDAVP washout and returned to basal levels within 75 min. In conclusion, the WT-10 cells mimic the vasopressin-regulated transcellular water transport and aquaporin-2 translocation as found in collecting duct cells to a great extent, and therefore constitute an in vitro cell model that can be used to study the regulation of transcellular water transport in detail and provide a simplified test system for screening putative aquaporin-2 blockers.
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PMID:Aquaporin-2 transfection of Madin-Darby canine kidney cells reconstitutes vasopressin-regulated transcellular osmotic water transport. 933 76

Vasopressin V2-receptor antagonists are promising agents for the use in water-retaining diseases. Potential renal mechanisms of action include effects on water permeability in the collecting duct as well as on electrolyte transport in the thick ascending limb of Henle's loop (TALH). To elucidate sites of action upstream of the distal tubule, e.g., in TALH, micropuncture experiments were performed in anesthetized rats during application of the V2-receptor antagonist SR 121463B. As compared to vehicle-treated rats, SR 121463B (0.3 mg/kg i.v.) did not affect mean arterial blood pressure (means +/- SEM, n=10 rats per group: 108+/-4 mmHg vs. 107+/-4 mmHg), whole kidney GFR (1.1+/-0.1 ml/min vs. 1.1+/-0.1 ml/min), or whole kidney fractional reabsorption (FR) of potassium (66+/-5% vs. 68+/-4%). The drug, however, reduced whole kidney FR of fluid (92+/-1% vs. 99+/-1%), increased urinary flow rate (84+/-7 microl/min vs. 8+/-1 microl/min) and electrolyte-free-water clearance (72+/-8 microl/min vs. 2+/-1 microl/min), and reduced urinary osmolality (148+/-11 mosmol/kg vs. 1,200+/-185 mosmol/kg). This pronounced diuretic response was associated with a minor reduction in whole kidney FR of sodium (99.6+/-0.1% vs. 99.9+/-0.1%) and chloride (98.3+/-0.2% vs. 98.9+/-0.1%). As compared to vehicle application, SR 121463B did not significantly alter single nephron GFR (39+/-2 nl/min vs. 39+/-1 nl/min, n=22 and 23 nephrons, respectively) or the FR up to the early distal tubule of fluid (76+/-2% vs. 76+/-1%), sodium (92+/-1% vs. 93+/-1%), potassium (91+/-1% vs. 90+/-1%) or chloride (90+/-1% vs. 91+/-1%). Together these data indicate a predominant aquaretic effect of SR 121463B which is located downstream of the early distal tubule. This response is compatible with blockade of vasopressin V2-receptors in the collecting duct and, as directly demonstrated by immunohistochemistry, subsequent retrieval of aquaporin-2 from apical plasma membrane, which inhibits water permeability and transport.
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PMID:Acute renal response to the non-peptide vasopressin V2-receptor antagonist SR 121463B in anesthetized rats. 1099 21


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