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

Whereas collecting duct epithelium in vivo is composed of principal and intercalated cells, we grew a pure principal cell epithelium using a new technique involving tissue culture. These principal cells were derived from collecting duct anlagen of newborn rabbits. We investigated the electrical properties of such epithelia in a newly designed lucite double-chamber with an inner opening of 0.08 cm2. Our observations were: mean transepithelial resistance Rte was 0.83 +/- 0.2 k omega cm2 at 37 degrees C and after preincubation in aldosterone; mean transepithelial potential difference Vte was low and variable under standard conditions and at room temperature but increased to -59.5 +/- 4.4 mV (sign referring to polarity of apical surface) after preincubation in 10(-6) mol/l aldosterone and at 37 degrees C; 10(-6) mol/l amiloride added to the apical perfusion fluid largely abolished this Vte while increasing Rte by 120%; experiments with 5 X 10(-3) mol/l BaCl2 in the apical perfusion fluid failed to change Rte and Vte significantly. This principal cell epithelium therefore has characteristics of a "tight" epithelium with active sodium transport; however, its electrical properties differ from those of the isolated perfused collecting duct segment.
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PMID:Electrical properties of renal collecting duct principal cell epithelium in tissue culture. 352 Apr 75

Segments of the outer medullary collecting duct were dissected from the outer stripe of the rabbit kidney (OMCDo) and perfused in vitro. The conductive properties of the tubule epithelium and individual cell membranes were determined by means of cable analysis and intracellular voltage-recording microelectrodes. The transepithelial voltage (VT) and resistance (RT) averaged -10.7 +/- 2.5 mV, lumen negative, and 28.5 +/- 2.9 k omega X cm (n = 27), respectively. Two cell types could be defined by their electrophysiological properties. One cell type (n = 7) had a mean basolateral membrane voltage (Vbl) of -30.1 +/- 2.4 mV, a fractional resistance of the apical membrane (fRa = Ra/Ra + Rbl) near unity (0.99 +/- 0.01), and a predominantly Cl(-)-selective basolateral cell membrane. The second cell type (n = 27) had a mean Vbl of -63.7 +/- 2.7 mV, a fRa of 0.81 +/- 0.02, and a predominantly K+-selective basolateral cell membrane. The present study focused on defining the conductive properties of this latter cell type. Amiloride (10(-5) M) and BaCl2 (2 mM) were used as probes of apical cell membrane Na+ and K+ conductive pathways, respectively. Amiloride increased fRa from 0.80 +/- 0.02 to 0.98 +/- 0.01 (n = 12), whereas BaCl2 increased fRa from 0.77 +/- 0.03 to 0.82 +/- 0.03 (n = 9). The conductive properties of the basolateral cell membrane were assessed by ion substitutions of the bath solution. A 10-fold increase in the bath [K+] depolarized Vbl by 34.9 +/- 1.9 mV (n = 16) in less than 1 s, indicating that this membrane was predominantly K+ selective.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Conductive properties of the rabbit outer medullary collecting duct: outer stripe. 394 27

Segments of outer medullary collecting duct were dissected from the inner stripe of the rabbit kidney (OMCDi) and perfused in vitro. The conductive properties of the tubule epithelium and individual cell membranes were determined by means of cable analysis and intracellular voltage-recording microelectrodes. In 35 tubules the transepithelial voltage (VT) and resistance (RT) averaged 17.2 +/- 1.4 mV, lumen positive, and 58.6 +/- 5.3 k omega X cm, respectively. The basolateral membrane voltage, (Vbl) was -29.2 +/- 2.1 mV (n = 23). The apical cell membrane did not contain appreciable ion conductances, as evidenced by the high values of apical cell membrane fractional resistance (fRa = Ra/Ra + Rb), which approached unity (0.99 +/- 0.01; n = 23). Moreover, addition of amiloride or BaCl2 to the tubule lumen was without effect on the electrical characteristics of the cell, as was a twofold reduction in luminal [Cl-]. The conductive properties of the basolateral cell membrane were assessed with bath ion substitutions. A twofold reduction in bath [Cl-] depolarized Vbl by 14.7 +/- 0.4 mV (theoretical, 17 mV), while a 10-fold increase in bath [K+] resulted in only a 0.9 +/- 0.4 mV depolarization (theoretical, 61 mV). Substituting bath Na+ with tetramethylammonium (from 150 to 75 mM) was without effect. Reducing bath [HCO-3] from 25 to 5 mM (constant PCO2) resulted in a steady-state depolarization of Vbl of 8.4 +/- 0.4 mV that could not be attributed to conductive HCO-3 movement. Thus, the basolateral cell membrane is predominantly Cl- selective.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Conductive properties of the rabbit outer medullary collecting duct: inner stripe. 398 56

We have previously found that arginine vasopressin (AVP) acts not only from the basolateral side but also from the luminal side of the rabbit cortical collecting duct (CCD). In the present study, we examined whether prostaglandin E2 (PGE2), another classic and potent modulator of the collecting duct functions, exerts luminal actions in the rabbit CCD perfused in vitro. Although luminal prostaglandin I2 was inert, luminal PGE2 (> 1 nM) induced transient hyperpolarization of transepithelial voltage followed by sustained depolarization in a dose-dependent manner. This action was preserved in the presence of basolateral PGE2, luminal AVP, or luminal BaCl2, but abolished by basolateral ouabain or luminal amiloride. Furthermore, unlike luminal AVP, luminal PGE2 suppressed Na transport and increased osmotic water permeability. The present study suggests that PGE2, similar to AVP but in a different fashion, modulates transepithelial transports from both luminal and basolateral sites in the CCD in vivo.
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PMID:Luminal prostaglandin E2 modulates sodium and water transport in rabbit cortical collecting ducts. 761 50

In the rat terminal inner medullary collecting duct (tIMCD), Na+ pump inhibition reduces transepithelial net acid secretion (JtAMM) [JH = total CO2 absorption (JtCO2)+ total ammonia secretion] and increases resting intracellular pH (pHi). The increase in pHi and reduction in JH that follow ouabain addition do not occur in the absence of NH4+ nor when NH4+ is substituted with another weak base. The purpose of this study was to explore the mechanism of the NH4(+)-dependent reduction in JtCO2 and increase in pHi that follow ouabain addition. We hypothesized that NH4+ enters the tIMCD cell through the Na(+)-K(+)-ATPase with proton release in the cytosol. To test this hypothesis, tIMCDs were dissected from deoxycorticosterone-treated rats and perfused in vitro with symmetrical physiological saline solutions containing 6 mM NH4Cl. Since K+ and NH4+ compete for a common binding site on the Na+ pump, increasing extracellular K+ should limit NH4+ (and hence net H+) uptake by the Na+ pump. Upon increasing extracellular K+ concentration from 3 to 12 mM, the NH4(+)-dependent, ouabain-induced increase in pHi and reduction in JtCO2 were attenuated. In the presence but not in the absence of NH4+, reducing Na+ pump activity by limiting Na+ entry reduced JtCO2 and attenuated ouabain-induced alkalinization. Ouabain-induced alkalinization was not dependent on the presence of HCO3-/CO2 and was not reproduced with BaCl2 or bumetanide addition. Therefore, ouabain-induced alkalinization is not mediated by the Na(+)-K(+)-2Cl- cotransporter or a HCO3- transporter and is not mediated by changes in membrane potential. In conclusion, on the basolateral membrane of the tIMCD cell, NH4+ uptake is mediated by the Na(+)-K(+)-ATPase. These data provide an explanation for the reduction in net acid secretion in the tIMCD observed following administration of amiloride or with dietary K+ loading.
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PMID:Ouabain reduces net acid secretion and increases pHi by inhibiting NH4+ uptake on rat tIMCD Na(+)-K(+)-ATPase. 943 73

cis-Diamminedichloroplatinum II (CDDP) is an antineoplastic drug against solid malignant tumors. However, its clinical use is limited by nephrotoxicity. CDDP also causes hypokalemia and in vivo microperfusion method have demonstrated that luminal CDDP increases K+ secretion by hyperpolarization of the transepithelial voltage difference through stimulating Na+ transport in the distal segments. However, there is no direct evidence for this mechanism. We therefore examined the effect of luminal CDDP on Na+ and K+ transport in the rabbit cortical collecting duct (CCD) using in vitro isolated tubular microperfusion. Luminal CDDP hyperpolarized the transepithelial voltage difference (V(T)) in a dose-dependent manner at concentrations from 10(-5) M to 10(-3) M and at 10(-3) M CDDP, V(T) was hyperpolarized from -11.6+/-2.3 mV to -16.6+/-3.3 mV (P<0.001). A concentration of 10(-5) M ouabain, 10(-4) M amiloride and 2 mM BaCl2 all completely abolished CDDP-induced hyperpolarization. To confirm the mechanism, Na+ and K+ flux were measured in the presence of 10(-3) M CDDP. CDDP decreased net K+ secretion from -22.2+/-5.7 to -15.2+/-2.9 pmol mm(-1) min(-1) (P<0.01) without any effect on the lumen-to-bath isotope flux of Na+ (52.6+/-10.6 to 52.1+/-10.7 pmol mm(-1) min(-1)). These data suggest that luminal CDDP hyperpolarizes V(T) primarily by inhibiting K+ conductance but did not influence Na+ transport of the luminal membrane. We conclude that the CCD does not play a role in CDDP-induced hypokalemia when CDDP is applied from the luminal side.
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PMID:The effect of cis-Diamminedichloroplatinum II on Na+ and K+ transport in the rabbit cortical collecting duct. 1047 66