scholarly journals Effect of chlorpropamide on water and urea transport in the inner medullary collecting duct

1991 ◽  
Vol 39 (1) ◽  
pp. 79-86 ◽  
Author(s):  
Antonino S. Rocha ◽  
Wong C. Ping ◽  
Lúcia H. Kudo
Keyword(s):  
Collecting Duct ◽  
Urea Transport ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct

The vasopressin-regulated urea transporter in renal inner medullary collecting duct

1990 ◽  
Vol 259 (3) ◽  
pp. F393-F401 ◽  
Author(s):  
M. A. Knepper ◽  
R. A. Star
Keyword(s):  
Apical Membrane ◽  
Collecting Duct ◽  
Water Channel ◽  
Toad Urinary Bladder ◽  
Urea Transport ◽  
Urea Transporter ◽  
Transport Pathway ◽  
Inner Medullary Collecting Duct ◽  
Urea Permeability ◽  
Medullary Collecting Duct

The terminal part of the inner medullary collecting duct (terminal IMCD) is unique among collecting duct segments in part because its permeability to urea is regulated by vasopressin. The urea permeability can rise to extremely high levels (greater than 100 x 10(-5) cm/s) in response to vasopressin. Recent studies in isolated perfused IMCD segments have established that the rapid movement of urea across the tubule epithelium occurs via a specialized urea transporter, presumably an intrinsic membrane protein, present in both the apical and basolateral membranes. This urea transporter has properties similar to those of the urea transporters in mammalian erythrocytes and in toad urinary bladder, namely, inhibition by phloretin, inhibition by urea analogues, saturation kinetics in equilibrium-exchange experiments, and regulation by vasopressin. The urea transport pathway is distinct from and independent of the vasopressin-regulated water channel. The increase in transepithelial urea transport in response to vasopressin is mediated by adenosine 3',5'-cyclic monophosphate and is associated with an increase in the urea permeability of the apical membrane. However, little is known about the physical events associated with the activation or insertion of urea transporters in the apical membrane. Because of the importance of this transporter to the urinary concentrating mechanism, efforts toward understanding its molecular structure and the molecular basis of its regulation appear to be justified.

Effect of peritubular hypertonicity on water and urea transport of inner medullary collecting duct

1992 ◽  
Vol 262 (3) ◽  
pp. F338-F347 ◽  
Author(s):  
L. H. Kudo ◽  
K. R. Cesar ◽  
W. C. Ping ◽  
A. S. Rocha
Keyword(s):  
Hydraulic Conductivity ◽  
Collecting Duct ◽  
Osmotic Gradient ◽  
Urea Transport ◽  
Perfusion Fluid ◽  
Cyclic Monophosphate ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
Series Of Experiments

The effect of bath fluid hypertonicity on hydraulic conductivity (Lp) and [14C]urea permeability (Pu) of the distal inner medullary collecting duct (IMCD) was studied in the absence and in the presence of vasopressin (VP) using the in vitro microperfusion technique of rat IMCD. In the first three groups of IMCD, we observed that in the absence of VP the Lp was not different from zero when the osmotic gradient was created by hypotonic perfusate and isotonic bath fluid, but it was significantly greater than 1.0 x 10(-6) cm.atm-1.s-1 when the osmotic gradient was created by hypertonic bath and isotonic perfusion fluid. The increase in Lp was observed when the hypertonicity of the bath fluid was produced by the addition of NaCl or raffinose, but no such effect was observed with urea. The stimulated effect of bath fluid hypertonicity on Lp was also observed in the IMCD obtained from Brattleboro homozygous rats in which VP is absent. The NaCl hypertonic bath increased the Pu in the absence of VP. In another series of experiments with VP (10(-10) M) we observed that the hypertonic bath fluid increased in a reversible manner the VP-stimulated Lp of distal IMCD. However, the NaCl hypertonicity of the bath fluid was not able to increase dibutyryladenosine 3',5'-cyclic monophosphate-stimulated Lp. The Pu stimulated by VP (10(-10) M) increased twofold when the bath fluid was hypertonic. Therefore hypertonicity of the peritubular fluid produced by the addition of NaCl or raffinose increases the Lp and Pu in the absence and in the presence of VP. No such effect was noted with the addition of urea.

scholarly journals Vasopressin regulation of multisite phosphorylation of UT-A1 in the inner medullary collecting duct

2015 ◽  
Vol 308 (1) ◽  
pp. F49-F55 ◽  
Author(s):  
Carol A. Hoban ◽  
Lauren N. Black ◽  
Ronald J. Ordas ◽  
Diane L. Gumina ◽  
Fadi E. Pulous ◽  
...  
Keyword(s):  
Apical Membrane ◽  
Collecting Duct ◽  
Phosphorylation Site ◽  
Urea Transport ◽  
Urea Transporter ◽  
Inner Medullary Collecting Duct ◽  
Camp Pathway ◽  
Multisite Phosphorylation ◽  
Medullary Collecting Duct ◽  
Stimulation Of

Vasopressin signaling is critical for the regulation of urea transport in the inner medullary collecting duct (IMCD). Increased urea permeability is driven by a vasopressin-mediated elevation of cAMP that results in the direct phosphorylation of urea transporter (UT)-A1. The identification of cAMP-sensitive phosphorylation sites, Ser486 and Ser499, in the rat UT-A1 sequence was the first step in understanding the mechanism of vasopressin action on the phosphorylation-dependent modulation of urea transport. To investigate the significance of multisite phosphorylation of UT-A1 in response to elevated cAMP, we used highly specific and sensitive phosphosite antibodies to Ser486 and Ser499 to determine cAMP action at each phosphorylation site. We found that phosphorylation at both sites was rapid and sustained. Furthermore, the rate of phosphorylation of the two sites was similar in both mIMCD3 cells and rat inner medullary tissue. UT-A1 localized to the apical membrane in response to vasopressin was phosphorylated at Ser486 and Ser499. We confirmed that elevated cAMP resulted in increased phosphorylation of both sites by PKA but not through the vasopressin-sensitive exchange protein activated by cAMP pathway. These results elucidate the multisite phosphorylation of UT-A1 in response to cAMP, thus providing the beginning of understanding the intracellular factors underlying vasopressin stimulation of urea transport in the IMCD.

Effect of insulin on water and urea transport in the inner medullary collecting duct

1994 ◽  
Vol 266 (3) ◽  
pp. F394-F399 ◽  
Author(s):  
A. J. Magaldi ◽  
K. R. Cesar ◽  
Y. Yano
Keyword(s):  
Water Transport ◽  
Collecting Duct ◽  
Water Channel ◽  
Polymyxin B ◽  
Dependent Manner ◽  
Urea Transport ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
Dose Dependent ◽  
Rule Out

The effect of insulin on water and urea transport was examined in normal isolated rat inner medullary collecting duct (IMCD). Hydraulic conductivity (Lp, x 10(-6) cm.atm-1.s-1), diffusional water permeability (Pdw, x 10(-5) cm/s) and [14C]urea permeability (x 10(-5) cm/s) were studied at 37 degrees C and pH 7.4. Insulin (6 x 10(-8) M; 200 microU/ml) added to the bath fluid enhanced Lp from 0.40 +/- 0.10 to 1.21 +/- 1.40 (P < 0.01) and Pdw from 42.40 +/- 3.40 to 58.50 +/- 5.00 (P < 0.02) and also stimulated Lp in a dose-dependent manner. In the presence of antidiuretic hormone (ADH)-stimulated Pdw (10 microU/ml), insulin increased Pdw even more. Prostaglandin E2 (10(-5) M) added to the bath reversibly increased insulin-induced Lp. Forskolin (10(-4) M) blocked the action of insulin. Colchicine (10(-4) M) and V1-receptor antagonist (10(-4) M) inhibited the development but not the maintenance of insulin-stimulated Pdw. Vanadate (2.5 x 10(-6) M) enhanced Pdw. Polymyxin B (10(-5) M) inhibited the insulin-stimulated Pdw, whereas in a glucose-free medium insulin did not enhance Pdw. Urea transport was not affected by insulin. These data suggest that insulin may enhance water transport, probably by stimulating glucose transporters, which would serve as a water channel. We cannot rule out the possibility that insulin may be eliciting existing ADH-like mechanisms of water transport, beyond the microtubule step, to establish water transport.

scholarly journals Epac Regulation of Urea Transport and the UT‐A1 Urea Transporter in Rat Inner Medullary Collecting Duct.

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Yanhua Wang ◽  
Janet D. Klein ◽  
Christopher F. Martin ◽  
Kimilia J. Kent ◽  
Susan M. Wall ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Urea Transport ◽  
Urea Transporter ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct

Nitric oxide inhibits superoxide-stimulated urea permeability in the rat inner medullary collecting duct

2003 ◽  
Vol 285 (6) ◽  
pp. F1160-F1167 ◽  
Author(s):  
Joseph Zimpelmann ◽  
Ningjun Li ◽  
Kevin D. Burns
Keyword(s):  
Nitric Oxide ◽  
Collecting Duct ◽  
Urea Transport ◽  
Superoxide Generation ◽  
No Donor ◽  
Inner Medullary Collecting Duct ◽  
Medullary Collecting Duct ◽  
Nos Inhibitor ◽  
Synthetic Capacity

The inner medullary collecting duct (IMCD) contains relatively high nitric oxide (NO) synthetic capacity, but the effect of NO on IMCD transport remains unclear. We determined the effect of NO on basal and vasopressin (AVP)-stimulated urea ( Purea) and water ( Pf) permeabilities in isolated, perfused rat IMCD. The NO donor S-nitroso- N-acetylpenicillamine (SNAP) increased cGMP production in IMCD, but neither SNAP (10–4 M) nor 8-BrcGMP (10–4 M), the cell-permeable analog of cGMP, affected basal or AVP-stimulated Purea. The free radical superoxide is produced by oxidases in the kidney and can interact with NO. To determine the effect of superoxide generation on transport, IMCDs were incubated with diethyldithiocarbamate (DETC; 10–3 M), the inhibitor of superoxide dismutase (SOD). DETC significantly increased basal and AVP-stimulated Purea (control: 28.7 ± 4.5 vs. DETC: 40.9 ± 6.2 × 10–5 cm/s; P < 0.001; n = 9). Preincubation of IMCD with SNAP or the SOD mimetic tempol completely inhibited DETC-stimulated Purea. DETC caused a significant increase in superoxide generation by IMCD, and this was blocked by SNAP. Incubation of IMCD with the NO synthase (NOS) substrate l-arginine blocked the stimulatory effect of DETC on Purea, and this was reversed by the neuronal NOS inhibitor 7-nitroindazole. In contrast, neither basal nor AVP-stimulated Pf was affected by NO donors or DETC. In summary, exogenous or endogenously produced NO does not affect basal urea transport in the IMCD but inhibits superoxide-stimulated Purea. In the inner medulla, superoxide generation by local oxidases may stimulate urea transport, and the role of endogenous NO may be to dampen this effect by decreasing superoxide levels.

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