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

Arginine vasopressin (AVP) increases the urea permeability of the rat terminal inner medullary collecting duct (IMCD) to levels much greater than can be explained by lipid-phase permeation or paracellular diffusion, suggesting the presence of an AVP-stimulated facilitated transport pathway. We tested whether inhibitors of facilitated urea transport in erythrocytes and toad bladder also inhibit urea transport in the isolated perfused IMCD. Apparent urea permeability (Purea) was determined by measuring the flux due to an imposed 5 mM concentration gradient. Phloretin (0.25 mM in lumen or bath) reversibly inhibited Purea. Phloretin, however, did not alter the osmotic water permeability. Urea analogues (200 mM) in the bath inhibited Purea (thiourea, 74% inhibition; methylurea 65%; acetamide 35%). Urea analogues in the lumen decreased Purea with the same order of potency. The inhibitory K1/2 for thiourea in the lumen was 27 +/- 2 mM and did not change with 10(-10) M AVP (28 +/- 3), despite a fourfold increase in Purea. We conclude the following. 1) Inhibitor actions on urea transport in the IMCD are similar to those in red blood cells and toad bladder, suggesting that the urea transporter could be a membrane protein similar to that in the other tissues. 2) Inhibition of Purea by phloretin without an effect on vasopressin-stimulated water permeability supports the view that the urea pathway is not the vasopressin-stimulated water channel. 3) The ability of AVP to increase Purea without an effect on the inhibitory K1/2 for thiourea indicates that AVP probably does not act by altering the binding affinity of individual transporters for urea.
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PMID:Inhibition of urea transport in inner medullary collecting duct by phloretin and urea analogues. 250 65

Using the in vitro microperfusion technique on isolated rat papillary collecting duct (PCD), we examined whether the glutaraldehyde-fixation method can be also applied to the mammalian collecting duct for preservation of the vasopressin-stimulated water and urea transport. Arginine vasopressin (AVP) at 10(-9) mol/l increased diffusional water permeability (Pdw) from 101.9 +/- 10.76 to 283.3 +/- 16.67 X 10(-7) cm2 s-1 (n = 8, P less than 0.01) and urea permeability (Purea) from 30.3 +/- 2.24 to 83.5 +/- 7.80 X 10(-7) cm2 s-1 (n = 8, P less than 0.01). Both parameters remained elevated after fixation with 0.1 mol/l glutaraldehyde even in the absence of AVP, with the values being 265.0 +/- 14.47 and 74.5 +/- 7.15 X 10(-7) cm2 s-1, respectively. Glutaraldehyde fixation did not affect the basal levels of Pdw or Purea. Phloretin at 2.5 X 10(-4) mol/l decreased glutaraldehyde-fixed AVP-stimulated Purea from 79.0 +/- 7.96 to 29.7 +/- 3.66 X 10(-7) cm2 s-1 (n = 4, P less than 0.01) and from 73.2 +/- 7.05 to 38.7 +/- 3.53 X 10(-7) cm2 s-1 (n = 4, P less than 0.01) when the drug was added to the lumen or to the bath, respectively. Phloretin also decreased glutaraldehyde-fixed non-stimulated Purea by 25-40%. However, this drug did not affect glutaraldehyde-fixed Pdw. These findings indicate that the glutaraldehyde fixation method can be applied to mammalian collecting tubules for studying vasopressin stimulated Pdw and Purea. Purea fixed by glutaraldehyde is functionally flexible and may be distinct from the water pathway.
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PMID:Effects of glutaraldehyde fixation on renal tubular function. I. Preservation of vasopressin-stimulated water and urea pathways in rat papillary collecting duct. 311 Jul 36

Partially because of facilitated transport of urea, urea permeability (Pu) of the outer medullary descending vasa recta (OMDVR) frequently exceeds sodium permeability by more than an order of magnitude. This study characterizes the OMDVR urea transporter. Application of the urea analogue thiourea (200 mM) to the abluminal surface of microperfused OMDVR inhibited Pu by 33%. When osmolarity due to thiourea was balanced by addition of mannitol or thiourea, similar results were obtained. Thiourea produced graded inhibition of Pu from 343 +/- 54 (SE) to 191 +/- 43 x 10(-5) cm/s as concentration was increased from 0 to 100 mM. The thiourea concentration needed for half-maximal inhibition was 19 mM. The abilities of urea analogues to reduce Pu were compared by addition of 50 mM concentrations to the bath and perfusate. Thiourea and methylurea produced 32 and 34% inhibition of Pu, respectively, whereas urea and acetamide produced only 3 and 11% inhibition, respectively. The transporter showed negligible saturation as the transmural urea gradient was increased from 0 to 200 mM. Phloretin and p-chloromercuribenzenesulfonate inhibited Pu in a concentration-dependent fashion. It is concluded that a transporter confers high Pu to OMDVR. Pu is equally high when measured by urea influx or efflux. Properties of the transporter are similar to those expressed by the inner medullary collecting duct.
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PMID:Characterization of the urea transporter in outer medullary descending vasa recta. 804 31

We measured the urea and NaCl permeabilities (Purea and PNaCl, respectively) of the following nephron segments from chinchilla: the upper part of the long-loop descending limb (from outer medulla, LDLu), the middle part of the long-loop descending limb (from outer 30% of the inner medulla, LDLm), the lower part of the long-loop descending limb (from deep inner medulla, LDLl), and the thin ascending limb (from deep inner medulla, ATL). We found that Purea (x10(-5) cm/s) was relatively low in the LDLu (3.3), but that the value was larger in the inner medullary thin descending limb (16.8 for LDLm and 47.6 for LDLl). The ATL had an even higher value (170). Phloretin, 0.25 mM, added to the peritubular bath had no effect on Purea of these segments, suggesting that the rapid transport rate is not due to a phloretin-sensitive facilitated transport pathway like that seen in the inner medullary collecting duct. PNaCl (x10(-5) cm/s) also increased with distance along the length of the thin descending limb (LDLu, 11.7; LDLm, 41.2; LDLl, 98.4; and ATL, 321). Calculations from NaCl dilution potential measurements showed that LDLu was Na+ permselective, whereas LDLl and ATL were Cl- permselective. High solute permeabilities in the inner medullary thin descending limb contradict a major requirement of the passive model of urinary concentration developed previously (J. P. Kokko and F. C. Rector, Jr. Kidney Int. 2: 214-223, 1972; and J. L. Stephenson. Kidney Int. 2: 85-94, 1972).
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PMID:In vitro perfusion of chinchilla thin limb segments: urea and NaCl permeabilities. 844 43