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)

We investigated the effect of cell shrinkage on whole-cell currents of M-1 mouse cortical collecting duct cells. Addition of 100 mM sucrose to an isotonic NaCl bath solution induced cell shrinkage and increased whole-cell currents within 5-10 min by approximately 12-fold. The effect was reversible upon return to isotonic solution and could also be elicited by adding 100 mM urea or 50 mM NaCl. Replacement of bath Na+ by K+, Cs+, Li+, or Rb+ did not significantly affect the stimulated inward current, but replacement by N-methyl-D-glucamine reduced it by 88.1 +/- 1.3% (n = 34); this demonstrates that hypertonicity activates a nonselective alkali cation conductance. The activation was independent of extra- and intracellular Ca2+, but 1 or 10 mM ATP in the pipette suppressed it in a concentration-dependent manner, indicating that intracellular ATP levels may modulate the degree of channel activation. Flufenamic acid (0.1 mM) and gadolinium (0.1 mM) inhibited the stimulated current by 68.7 +/- 5.9% (n = 9) and 32.4 +/- 11.7% (n = 6), respectively, whereas 0.1 mM amiloride had no significant effect. During the early phase of hypertonic stimulation single-channel transitions could be detected in whole-cell current recordings, and a gradual activation of 30 and more individual channels with a single-channel conductance of 26.7 +/- 0.4 pS (n = 29) could be resolved. Thus, we identified the nonselective cation channel underlying the shrinkage-induced whole-cell conductance that may play a role in volume regulation.
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PMID:Hypertonicity activates nonselective cation channels in mouse cortical collecting duct cells. 754 4

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

We investigated immunohistochemical localization of V2 vasopressin receptor along the nephron using a specific polyclonal antibody. Staining was observed in some of thick ascending limbs and all of principal and inner medullary collecting duct (IMCD) cells. Not only basolateral but also luminal membrane was stained in collecting ducts, especially in terminal IMCD (tIMCD). To learn the functional role of luminal V2 receptor in tIMCD, we studied the luminal effects of arginine vasopressin (AVP) on osmotic water permeability (Pf), urea permeability (Pu), and cAMP accumulation using isolated perfused rat tIMCD. In the absence of bath AVP, luminal AVP caused a small increase in cAMP accumulation, Pf and Pu, confirming the presence of V2 receptor in the lumen of tIMCD. In contrast, luminal AVP inhibited Pf and Pu by 30-65% in the presence of bath AVP by decreasing cAMP accumulation via V1a or oxytocin receptors and by an unknown mechanism via V2 receptors in the luminal membrane of tIMCD. These data show that V2 receptors are localized not only in the basolateral membrane but also in the luminal membrane of the distal nephron. Luminal AVP acts as a negative feedback system upon the basolateral action of AVP in tIMCD.
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PMID:Immunohistochemical localization of V2 vasopressin receptor along the nephron and functional role of luminal V2 receptor in terminal inner medullary collecting ducts. 756 68

In the vasopressin-stimulated inner medullary collecting duct (IMCD), urea is transported through a pathway which is distinct from a water channel. Therefore, no frictional interaction between urea and water should occur at the membrane level, and the reflection coefficient for urea must be close to unity. However, the presence of unstirred layers in the vicinity of membranes causes solute concentration polarization, leading to an underestimation of the reflection coefficient (apparent reflection coefficient). When the value is determined across the perfused renal tubular wall, the intracellular space also constitutes an unstirred layer. The profile of solute and water transport across the system consisting of two membranes and the interposed intracellular space was simulated by a computer to examine the effect of unstirred layer on the value of apparent reflection coefficient. The model demonstrated that the imposed osmotic gradient across the tubular epithelial is decreased at each membrane interface. Under conditions of minimal unstirred layers in the bathing fluid, the existence of the intracellular constraints to diffusion cause considerable underestimation of the reflection coefficient. The higher the membrane permeability of urea and the smaller the diffusion coefficient of urea in the intracellular space, the greater becomes the magnitude of the underestimation. Thus, the measured apparent reflection coefficient for urea may become significantly less than the estimated value, leading to a reduction of the effective transmural osmotic driving force.
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PMID:Effect of intracellular unstirred layer on apparent reflection coefficient for urea in inner medullary collecting duct: a computer simulation. 762 Aug 57

We conducted this study to determine what receptor mediates the effect of oxytocin to increase osmotic water permeability (Pf) in the rat inner medullary collecting duct (IMCD). Reverse transcription-polymerase chain reaction (RT-PCR) experiments demonstrated that mRNA for both the oxytocin receptor and the V2 receptor is present in the rat terminal IMCD. In isolated perfused IMCD segments, we found that the V2 vasopressin receptor antagonist [d(CH2)5(1),D-Ile2,Ile4,Arg8]vasopressin, but not oxytocin receptor antagonists, blocked the hydrosmotic response to 200 pM oxytocin. The selective oxytocin receptor agonist [Thr4,Gly7]oxytocin did not increase water permeability. Oxytocin also increased urea permeability in IMCD segments. Studies in IMCD suspensions showed that oxytocin increases adenosine 3',5'-cyclic monophosphate production in a dose-dependent fashion with a half-maximal (EC50) response at 5.2 nM. The dose-response curves were virtually identical for IMCD suspensions from Sprague-Dawley rats and Brattleboro rats. The oxytocin dose-response curve was displaced to the right of the vasopressin dose-response curve (EC50, 0.44 nM). From these results, we conclude that the V2 receptor mediates the hydrosmotic action of oxytocin in rat IMCD.
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PMID:Oxytocin as an antidiuretic hormone. II. Role of V2 vasopressin receptor. 763 34

The present study was undertaken to explore the acute effect of hyperosmolality on the response of cultured rat inner medullary collecting duct (IMCD) cells to atrial natriuretic peptide (ANP). In contrast to the stimulatory effect of chronic incubation (12 h) in hypertonic medium, it was found that short-term incubation (< 2 h) reversibly suppressed the ANP-dependent cyclic guanosine monophosphate (cGMP) production. Urea, NaCl and mannitol were equi-potent as the osmolyte in suppressing the ANP-dependent cGMP production. Receptor binding assay revealed that hyperosmolality induced a rapid and marked reduction of the maximum binding (Bmax) of ANP without a significant change of the dissociation constant (Kd). Pretreatment with protein kinase C inhibitors (calphostin-C, staurosporin) or with cytoskeleton modulators (cytochalasin-B, colchicine) did not affect the inhibitory effect of hyperosmolality. In conclusion, acute hypertonicity inhibited the ANP-induced cGMP production in contrast to chronic hypertonicity, and reduction of the number of ANP binding sites was considered to be a mechanism responsible for the inhibitory effect of hypertonicity.
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PMID:Hyperosmolality rapidly reduces atrial-natriuretic-peptide-dependent cyclic guanosine monophosphate production in cultured rat inner medullary collecting duct cells. 766 80

In this paper we describe a mathematical model of the renal inner medulla based on a previously proposed model [A.S. Wexler, R.E. Kalaba, and D.J. Marsh. Am. J. Physiol. 260 (Renal Fluid Electrolyte Physiol. 29): F368-F383, 1991] in which in the inner medullary ascending thin limb of Henle's loop (ATL) and collecting duct (CD) exchange with a local capillary node with the reabsorbed water and solutes flowing radially toward a central vascular bundle. Our model differs in that ascending and descending vasa recta and surrounding interstitial space are replaced by a central core. Our analysis of the coupled ATL-CD system shows that it is theoretically capable of transporting NaCl out of the ATL into the central vascular space (approximated by the central core) against a concentration gradient, which in the absence of radial diffusion can be arbitrarily large. By numerical solution of the model with the radial diffusion coefficient (D(r)) for NaCl of 0, we find that the ATL can be more than 100 mosmol/l hypotonic with respect to the core. We also find that with restricted diffusion the osmolality of the CD at the papilla is significantly greater than that of the loop of Henle. As D(r) approaches the diffusion coefficient of NaCl in free solution, the osmolality of the loop increases and that of the CD decreases. Thus, overall, contrary to intuitive expectations, the radial separation and uphill transport of NaCl do not give any significant increase in loop concentration, which depends primarily on the quantity of urea reabsorbed from the CD.
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PMID:Convective uphill transport of NaCl from ascending thin limb of loop of Henle. 773 25

In this study we extend the analysis of the preceding two studies [J. L. Stephenson, J. F. Jen, H. Wang, and R. P. Tewarson. Am. J. Physiol. 268 (Renal Fluid Electrolyte Physiol. 37): F698-F709, 1995; and J. F. Jen, H. Wang, R. P. Tewarson, and J. L. Stephenson. Am. J. Physiol. 268 (Renal Fluid Electrolyte Physiol. 37): F000-F000, 1995] to a model that includes vasa recta. Distribution of nephron and vasa recta lengths is represented by shunting from descending to ascending flow. It is found that the effect of radial separation of structures on concentrating ability is closely linked to vasa recta flow. With minimal or no vasa recta flow the extent of radial mixing has little effect on concentrating ability. As vasa recta flow increases, concentrating ability is decreased by radial mixing. Convective uphill transport of NaCl is again observed, but concentrating ability appears to depend primarily on urea delivery to the inner medulla from the collecting duct rather than on the mechanism of salt transport out of thin ascending limb. Central core models give an upper bound on concentrating ability but do not attain the maximum urine osmolality of the rat with experimental values of tubular permeabilities.
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PMID:Effect of vasa recta flow on concentrating ability of models of renal inner medulla. 773 27

Prolonged fluid restriction in rats is accompanied by functional modifications of the terminal part of the inner medullary collecting duct (IMCD) revealed by a sustained increase in arginine vasopressin (AVP)-independent transepithelial osmotic water permeability (PTE) in vitro. The cellular basis of this adaptation was explored in isolated and perfused terminal IMCDs of Sprague-Dawley rats using video and fluorescence microscopy. Basolateral membrane osmotic water permeability (Posm), transcellular Posm, and PTE were measured in quick sequence in every tubule. They were expressed per unit area of basolateral membrane corrected for infoldings, based on previous stereological studies and assuming no major change in membrane surface area between hydrated and dehydrated animals. Compared with IMCDs of rats with a high water intake, IMCDs of rats deprived of fluid for 36 h displayed a significantly higher basal PTE (24.9 +/- 5.1 vs. 6.1 +/- 0.6 microns/s), a similar basolateral Posm, and a higher transcellular Posm, implying a higher permeability of the apical membrane, despite the absence of exogenous AVP. However, when IMCDs of thirsted rats were exposed to AVP in vitro, their transcellular Posm (36.0 +/- 2.4 microns/s) was significantly smaller than their PTE determined simultaneously (51.8 +/- 7.1 microns/s), suggesting that part of the water flow may follow a paracellular route. A change in paracellular pathways was supported by higher apparent permeabilities to [14C]sucrose (0.85 +/- 0.27 vs. 0.28 +/- 0.04 x 10(-5) cm/s) and to [methoxy-3H]inulin (0.25 +/- 0.04 vs. 0.14 +/- 0.03 x 10(-5) cm/s) in IMCDs of thirsted rats. The nonelectrolyte permeabilities were affected neither by AVP nor by urea-rich bathing solutions. We conclude that in vivo factors related to dehydration produce a conditioning effect on terminal IMCD, which includes stabilization of the apical membrane in a state of high Posm and opening up of paracellular pathways revealed by a higher permeability to water and nonelectrolytes. The role of these adaptive phenomena remains unclear but may pertain to the sudden transitions between antidiuresis and diuresis.
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PMID:Adaptation of inner medullary collecting duct to dehydration involves a paracellular pathway. 784 Feb 48

The inner medullary collecting duct (IMCD) is a major target site of atrial natriuretic peptide (ANP) for diuresis and natriuresis, and it is in a hypertonic condition made by the renal countercurrent multiplication system. We investigated the effects of hyperosmolality on ANP-stimulated cGMP generation in IMCD and glomerulus. Hypertonic solutions (490 and 690 mOsm/kg.H2O) were made by adding NaCl or urea to isotonic solution (290 mOsm/kg.H2O). Hypertonicity of 490 mOsm/kg.H2O using NaCl reduced both ANP-stimulated guanylate cyclase activity (from 7.7 +/- 1.1 to 4.1 +/- 0.5 fmol/mm/5 min) and cGMP generation (from 1.35 +/- 0.18 to 0.48 +/- 0.20 fmol/mm/3 min) in IMCD. Hypertonicity of 690 mOsm/kg.H2O using NaCl did not further reduce ANP-stimulated cGMP generation in IMCD. Hypertonicity using urea also inhibited ANP-stimulated guanylate cyclase activity and cGMP generation in IMCD. On the other hand, hypertonicity using NaCl stimulated AVP-stimulated cAMP generation in IMCD, while hypertonicity using urea reduced it. In glomeruli, hyperosmolality of 490 mOsm/kg.H2O using NaCl also reduced ANP-stimulated cGMP generation, and hypertonicity of 690 mOsm/kg.H2O using NaCl further reduced it. In summary, hyperosmolality using NaCl and urea inhibited ANP-sensitive guanylate cyclase activity and cGMP generation both in IMCD and glomeruli. However, the mechanisms at work may be different between NaCl and urea.
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PMID:Effects of hyperosmolality on ANP-stimulated cGMP generation in rat inner medullary collecting duct. 791 40


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