Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

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

Functionally isolated segments of rat colon and rectum were perfused in situ in a closed loop system. Rectum was defined as the lower 25--35% of the length of large intestine (cecum excluded). Perfusion conditions were optimized at 0.5 ml.min-1 and 3 cm H2O luminal pressure. Variation of perfusion rate between 0.2 and 2 ml.min-1 did not influence net volume transport (JNV). Luminal distension following elevation of hydrostatic pressure to 18 cm H2O reversibly increased Jnv. Under control conditions Jnv and Na+-transport rates (JnNa) of colon were 2--3 times higher than those of rectum. In colon transepithelial electrical potential difference (psims) was time independent --12 mV (lumen negative) whereas rectal psims increased with time from --6 mV, reaching a plateau of --67 mV within 6 h. Amiloride 10(-4) mol.l-1 had no effect on psims, Jnv, and JnNa in colon but did slightly depress K+-secretion in colon descendens. In contrast, psims in rectum was dose-dependently depressed, being reversed to +7 mV at 10(-4) mol.l-1. Jnv and JnNa were decreased by half. Acetazolamide in addition to amiloride lowered the positive post-amiloride rectal psims by half. Adrenalectomy had no effect on colonic psims, but abolished psims of the rectum. A single dose of 40 microgram.kg-1 b.w. aldosterone during the experiment restored the typical time course of rectal psims, but did not affect psims in colon. It is concluded that aldosterone induces an amiloride-sensitive Na+-pathway only in rectum, but not in colon, and that colon and rectum differ basically in their transport properties, quantitatively as well as qualitatively, as do the kidney distal convoluted tubule and the cortical collecting duct.
...
PMID:Segmental heterogeneity of epithelial transport in rat large intestine. 56 27

Using the shrinking droplet method and simultaneous perfusion of the peritubular capillaries the isotonic reabsorption of Ringer's solution from the papillary collecting ducts was measured. Under control conditions the volume reabsorption from the papillary collecting ducts was Jv +/- SE = 2.6 +/- 0.1 . 10(-5) cm3 . cm-2 . s-1. In rats which were on low Na+ diet, Jv increased to 127%, and in adrenalectomized animals it decreased to 34% of the control value. Three hours after a;ocatopm pf a;dpsterpme om tje adrenalectomized animals Jv was partially restored to 63% of control rats. Amiloride 10(-4) M, added to the luminal perfusate, produced a strong inhibition of Jv (to 32% of control). Acetazolamide, 10(-4) M, added to both perfusates, reduced Jv very strongly (to 40% of control), while omission of bicarbonate reduced it only to 77% of control. Acetazolamide, added to bicarbonate-free perfusates, did not result in a significant further reduction of Jv. The data indicate that the Na+ reabsorption from the papillary collecting duct is controlled by mineralocorticoids. Furthermore, they suggest the existence of two transport mechanisms in the luminal cell membrane: 1. An amiloride-sensitive entry step and 2. an entry step via a Na+-H+-countertransport mechanism, the latter being less important.
...
PMID:Sodium reabsorption in the papillary collecting duct of rats. Effect of adrenalectomy, low Na+ diet, acetazolamide, HCO-3-free solutions and of amiloride. 57 Nov 3

The present study was undertaken to determine whether the change in cellular Na+ concentration ( [Na+]i) or cellular pH (pHi) is essential for the modulation by Na+/H+ antiporter of the cellular action of arginine vasopressin (AVP) in renal inner medullary collecting duct cells in culture. Extracellular Na+ depletion promptly decreased [Na+]i from 15.8 to 5.4 mM (P less than 0.01), which was closely related to the decrease in pHi (7.19 to 6.97; P less than 0.01). In the presence of 0.5 mM 3-isobutyl-1-methylxanthine, AVP increased cellular cAMP production in a dose-dependent manner. This was significantly blunted in the Na(+)-depleted cells (1 nM AVP; 481.9 vs. 341.0 fmol/micrograms protein; P less than 0.01). When cells were incubated with the Na(+)-depleted medium containing 25 mM NaHCO3, [Na+]i decreased promptly, but the pHi remained unchanged. Under this condition, the AVP-induced increase in cellular cAMP production was not altered (1 nM AVP; 390.9 vs. 334.8 fmol/micrograms protein). Also, after the Na(+)-depleted cells were incubated in 20 mM NH4Cl, which promptly normalized pHi despite the decreased [Na+]i, the response of cAMP production to AVP was restored. Amiloride (1 x 10(-5)-1 x 10(-3) M), which blocks the Na+/H+ exchange, decreased pHi and AVP- and forskolin-induced cAMP production in a dose-dependent manner. These results indicate that the decrease in [Na+]i promptly inhibits AVP-induced cAMP production mediated through the reduction in pHi in renal inner medullary collecting duct cells.
...
PMID:pH dependence of inhibition of arginine vasopressin-induced adenosine 3',5'-monophosphate production by cellular sodium depletion in rat renal inner medullary collecting duct cells in culture. 130 26

The electrophysiological properties of the hamster mid-inner medullary collecting duct (IMCD2) cells were examined in isolated and perfused preparations by intracellular impalement with conventional 1 mol/l KCl microelectrodes and cable analysis. The transmural voltage (VT) was not different from 0 mV, while the basolateral transmembrane voltage (VB) was -81.7 +/- 0.91 mV (n = 221). The transmural resistance (RT) was 109 omega cm2, indicating that the IMCD2 is composed of tight epithelia. The fractional apical membrane resistance (fRA) was 0.98 +/- 0.003 (n = 10). Abrupt changes in the luminal concentration of Na+, K+ or Cl- did not alter the apical membrane voltage (VA) or VT, and neither 2 mmol/l Ba2+ nor 10 mumol/l amiloride in the lumen affected VA and VT. Moreover, pretreatment of hamsters with deoxycorticosterone acetate (5 mg/kg, s.c.) for 10-14 days caused only a very small change in VT in the negative direction. Amiloride in the lumen increased RT and increased the voltage divider ratio very slightly. However, an abrupt increase in K+ concentration in the bath from 5 mmol/l to 50 mmol/l or addition of 2 mmol/l Ba2+ to the bath depolarized the basolateral membrane by 39 mV and 29 mV, respectively. In the presence of 2 mmol/l Ba2+ in the bath, a reduction of HCO3- concentration from 25 mmol/l to 2.5 mmol/l depolarized VB by 20.4 mV. No Cl- conductance was demonstrated in the basolateral membrane.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Electrophysiological study of inner medullary collecting duct of hamsters. 216 31

Transmembrane sodium transport pathways were studied in principal and intercalated cells of the isolated perfused rabbit cortical collecting duct. Intracellular electrolyte concentrations in individual collecting duct cells were measured by electron microprobe analysis during blockage of basolateral Na-K-ATPase by ouabain and simultaneous inhibition of sodium entry across the apical and/or basolateral cell membrane. In principal cells the ouabain-induced rise in cell sodium concentration could only partially be blocked by amiloride (10(-4) mol/l) in the perfusion fluid. Amiloride (10(-3) mol/l) added to the bathing solution produced a further, significant reduction of sodium influx. In principal cells the ouabain-induced increase in sodium concentration was completely prevented by amiloride in the perfusion solution in combination with omission of sodium from the peritubular bathing solution. In intercalated cells ouabain caused a less pronounced increase in sodium concentration than in principal cells. Neither amiloride in the perfusate, nor amiloride in both bathing and perfusion solution, significantly reduced the ouabain-induced rise in intercalated cell sodium concentration. These results indicate that in principal cells amiloride-sensitive sodium channels constitute the predominant pathway for sodium entry across the apical cell membrane. In addition, substantial amounts of sodium enter principal cells across the basolateral cell membrane, probably via Na-H exchange. Finally, the data suggest that in intercalated cells sodium channels and the Na-H exchange are sparse or even absent.
...
PMID:Sodium entry routes in principal and intercalated cells of the isolated perfused cortical collecting duct. 216 37

To examine the mechanisms of H+ transport in the mid-inner medullary collecting duct of hamsters, we measured the intracellular pH (pHi) in the in vitro perfused tubules by microscopic fluorometry using 2',7'-bis(carboxyethyl)-carboxyfluorescein (BCECF) as a fluorescent probe. In the basal condition, pHi was 6.74 +/- 0.04 (n = 45) in HCO3(-)-free modified Ringer solution. Either elimination of Na+ from the bath or addition of amiloride (1 mM) to the bath produced a reversible fall in pHi. After acid loading with 25 mM NH4Cl, pHi spontaneously recovered with an initial recovery rate of 0.096 +/- 0.012 (n = 23) pH unit/min. In the absence of ambient Na+, after removal of NH+4, the pHi remained low (5.95 +/- 0.10, n = 8) and showed no signs of recovery. Subsequent restoration of Na+ only in the lumen had no effect on pHi. However, when Na+ in the bath was returned to the control level, pHi recovered completely Amiloride (1 mM) in the bath completely inhibited the Na(-)-dependent pHi recovery. Furthermore, elimination of Na+ from the bath, but not from the lumen, decreased pHi from 6.97 +/- 0.07 to 6.44 +/- 0.05 (n = 12) in the HCO3-/Ringer solution or 6.70 +/- 0.03 to 6.02 +/- 0.5 pH unit/min in the presence of CO2/HCO3-, whereas it did not recover in the absence of CO2/HCO3-.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Mechanisms of intracellular pH regulation in the hamster inner medullary collecting duct perfused in vitro. 217 46

Amiloride, triamterene, and the spirolactones are potassium-sparing diuretics which act on the distal parts of the nephron, from the late distal tubule to the collecting duct. In these segments, active sodium reabsorption occurs through the following mechanism: sodium ions enter the cell through specific channels present in the luminal membrane and are extruded out of the cell into the peritubular medium by a sodium-potassium exchange pump, the Na-K-ATPase. Amiloride in micromolar concentrations reduces the sodium transport by blocking the luminal membrane sodium channel. Triamterene has a similar effect, although with a lower affinity; the available studies do not allow to determine if an inhibitory effect of triamterene on the Na-K-ATPase plays an additional role in its diuretic action. The spirolactones are competitive inhibitors of aldosterone, the mineralocorticoid hormone which promotes sodium reabsorption by increasing both the number of active sodium channels in the luminal membrane and the number of active Na-K pumps in the peritubular membrane. By the inhibitory effect on the electrogenic sodium transport, amiloride, triamterene, and the spirolactones decrease the lumen-negative transepithelial potential difference. This reduces the driving force for potassium movement into the tubular lumen and thus decreases potassium excretion.
...
PMID:Potassium-sparing diuretics. 245 8

Ion channels in the apical membrane of rat inner medullary collecting duct (IMCD) cells in primary culture were studied with the patch-clamp technique. A 27.5 +/- 1.2 pS non-selective cation channel was characterized in inside-out patches. The channel did not discriminate between Na+ and K+ (n = 8) and had a Na permeability-to-Cl permeability (PNa:PCl) ratio of 13:1 (n = 3). Amiloride (5 x 10(-7) M, n = 5) on the extracellular side of the membrane inhibited channel activity 10-fold at negative membrane voltages (voltage refers to cell interior with respect to patch pipette). This diuretic decreased the mean open time and increased the mean closed time without altering single-channel conductance. Voltage-dependent inhibition of this channel by amiloride distinguishes its behavior from other known nonselective cation channels. Neither voltage, Ba2+ (1 mM), tetraethylammonium (5 mM) nor changes in the bath pH (6.1 to 8.0) altered channel activity. Although the channels were active in 41% of the patches in the inside-out configuration, with a percent open time lying between 35 and 60 (-70 to +60 mV), channels were only active in 9% of the cell-attached patches. In preliminary microelectrode studies we have observed an amiloride-inhibited conductance in the apical membrane of isolated and perfused rat IMCD. Therefore, this novel nonselective cation channel identified in IMCD cells in culture may represent the amiloride-sensitive conductance observed in isolated and perfused IMCD and may mediate electrogenic Na+ absorption.
...
PMID:Amiloride-sensitive cation channel in apical membrane of inner medullary collecting duct. 245 28

The inner medullary collecting duct (IMCD) effects net sodium reabsorption under the control of volume regulatory hormones, including atrial natriuretic peptides (ANP). These studies examined the mechanisms of sodium transport and its regulation by ANP in fresh suspensions of IMCD cells. Sodium uptake was inhibited by amiloride but insensitive to furosemide, bu-metanide, and hydrochlorthiazide. These results are consistent with uptake mediated by a sodium channel or Na+/H+ exchange. To determine the role of sodium channels, cells were hyperpolarized by preincubation in high potassium medium followed by dilution into potassium-free medium. Membrane potential measurements using the cyanine dye, Di(S)-C3-5 verified a striking hyperpolarization of IMCD cells using this protocol. Hyperpolarization increased the apparent initial rate of sodium uptake fourfold. Amiloride and ANP inhibited potential-stimulated sodium uptake 73% and 65%, respectively; the two agents together were not additive. Addition of 5 mM sodium to hyperpolarized cells resulted in a significant amiloride-sensitive depolarization. Half-maximal inhibition of potential-driven sodium uptake occurred at 3 X 10(-7) M amiloride, and 5 X 10(-11) M ANP. We conclude that sodium enters IMCD cells via a conductive, amiloride-sensitive sodium channel, which is regulated by ANP. ANP inhibition of luminal sodium entry in the IMCD appears to contribute to the marked natriuretic effect of this hormone in vivo.
...
PMID:Atrial natriuretic peptides inhibit conductive sodium uptake by rabbit inner medullary collecting duct cells. 245 85

Amiloride-sensitive Na+ channels were localized in semithin frozen sections of rat renal medullary collecting ducts, using polyclonal antibodies directed against purified bovine kidney Na+ channel protein. The apical plasma membrane of collecting duct principal cells was heavily stained by indirect immunofluorescence, whereas intercalated cells were negative. Basolateral plasma membranes of both cell types were unstained, as were subapical vesicles in the cytoplasm of these cells. In the thick ascending limb of Henle, some scattered granular fluorescence was seen in the cytoplasm and close to the apical pole of epithelial cells, suggesting the presence of antigenic sites associated with some membrane domains in these cells. No staining was detected in thin limbs of Henle, or in proximal tubules in the outer medulla. These results show that amiloride-sensitive sodium channels are located predominantly on the apical plasma membrane of medullary collecting duct principal cells, the cells that are involved in Na+ homeostasis in this region of the kidney.
...
PMID:Immunocytochemical localization of Na+ channels in rat kidney medulla. 253 28


1 2 3 4 5 Next >>

---