UNIPROT:P41181 - FACTA Search

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

Although vasopressin V1 receptors have been shown to exist in both luminal and basolateral membranes of rabbit cortical collecting duct (CCD), exact cell types having V1 receptors remain unestablished. To identify the distribution of V1 receptor by cytoplasmic Ca2+ response, we utilized the confocal imaging system in the microperfused rabbit CCD. Basolateral application of arginine vasopressin (AVP) increased [Ca2+]i mainly in one group of cells which were not stained by fluorescein-isothiocyanate-conjugated peanut agglutinin. Luminal application of AVP increased [Ca2+]i in the same cells which responded to basolateral AVP. These findings provide evidence that V1 receptors, as defined by the [Ca2+]i response, exist in both luminal and basolateral membranes of the rabbit principal cell.
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PMID:Cell Ca2+ response to luminal vasopressin in cortical collecting tubule principal cells. 819 83

Low protein diets reverse the urea concentration gradient in the renal inner medulla. To investigate the mechanism(s) for this change, we studied urea transport and cell ultrastructure in initial and terminal inner medullary collecting ducts (IMCD) from rats fed 18% protein or an isocaloric, 8% protein diet for 4 wk. Serum urea, aldosterone, and albumin were significantly lower in rats fed 8% protein, but total protein and potassium were unchanged. Vasopressin stimulated passive urea permeability (Purea) threefold (P < 0.05) in initial IMCDs from rats fed 8% protein, but not from rats fed 18% protein. Luminal phloretin reversibly inhibited vasopressin-stimulated Purea. However, in terminal IMCDs from rats fed either diet, vasopressin stimulated Purea. Net transepithelial urea flux (measured with identical perfusate and bath solutions) was found only in initial IMCDs from rats fed 8% protein. Reducing the temperature reversibly inhibited it, but phloretin did not. Electron microscopy of initial IMCD principal cells from rats fed 8% protein showed expanded Golgi bodies and prominent autophagic vacuoles, and morphometric analysis demonstrated a marked increase in the surface density and boundary length of the basolateral plasma membrane. These ultrastructural changes were not observed in the terminal IMCD. Thus, 8% dietary protein causes two new urea transport processes to appear in initial but not terminal IMCDs. This is the first demonstration that "active" urea transport can be induced in a mammalian collecting duct segment.
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PMID:Low protein diet alters urea transport and cell structure in rat initial inner medullary collecting duct. 822 60

In the rabbit cortical collecting duct (CCD) perfused in vitro, we recently found that luminal arginine vasopressin (AVP) hyperpolarizes the transepithelial voltage (Vt) and inhibits the hydrosmotic effect of basolateral AVP. The present study was undertaken to characterize the apical receptor of the CCD for AVP. In contrast to AVP, luminal application of 1-desamino-8-D-arginine vasopressin (DDAVP), a V2 agonist, did not significantly induce hyperpolarization. Luminal oxytocin (OXT) hyperpolarized Vt, interfering with the effect of superimposed luminal AVP, whereas [Thr4,Gly7]OXT, an OXT agonist, did not reproduce the effect of OXT. The effects of luminal AVP and OXT were abolished by [d(CH2)5,Tyr(Me)]-AVP, a V1 antagonist. Finally, luminal applications of AVP metabolite neuropeptides, pGlu-Asn-Cys(Cys)-Pro-Arg and pGlu-Asn-Cys(Cys)-Pro-Arg-Gly-NH2, were without effect on Vt. These data suggest that luminal AVP induces hyperpolarization through an apical V1 receptor but not through a V2 receptor or an OXT receptor.
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PMID:Functional evidence for an apical V1 receptor in rabbit cortical collecting duct. 845 59

This study evaluated the role of H-K-adenosinetriphosphatase (H-K-ATPase) with chronic metabolic acidosis (CMA) in intercalated cells (ICs) of rabbit cortical collecting duct (CCD). CMA was induced by replacing drinking water with 75 mM NH4Cl in 5% sucrose for 10-14 days. CCDs isolated from CMA and control rabbits were split open and exposed to the intracellular pH (pHi) indicator 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. In N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered solutions, the resting pHi in ICs was similar for both groups. K-dependent pHi recovery (5 mM K, 140 mM N-methyl-D-glucamine) was monitored in response to a pulse of NH4Cl (10 mM). The K-dependent pHi recovery rate was threefold higher in CMAICs compared with controls and was abolished with the gastric H-K-ATPase inhibitor, Sch-28080 (10(-5) M). Polarity of the H-K-ATPase was studied in microperfused CMA and control CCDs. Luminal K-dependent pHi recovery was monitored in response to an acute pulse of NH4Cl in individual peanut lectin agglutinin (PNA)-binding ICs. The apical Sch-28080-inhibitable K-dependent pHi recovery rate was significantly greater in CMA ICs than control ICs. In summary, CMA enhances functional activity of an apical H-K-ATPase in PNA-binding ICs of rabbit CCD.
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PMID:Stimulation of apical H-K-ATPase in intercalated cells of cortical collecting duct with chronic metabolic acidosis. 878 Feb 58

A mathematical model of the inner medullary collecting duct (IMCD) of the rat has been developed that is suitable for simulating luminal buffer titration and ammonia secretion by this nephron segment. Luminal proton secretion has been assigned to an H-K-ATPase, which has been represented by adapting the kinetic model of the gastric enzyme by Brzezinski et al. (P. Brzezinski, B. G. Malmstrom, P. Lorentzon, and B. Wallmark. Biochim. Biophys. Acta 942: 215-219, 1988). In shifting to a 2 H+:1 ATP stoichiometry, the model enzyme can acidify the tubule lumen approximately 3 pH units below that of the cytosol, when luminal K+ is in abundance. Peritubular base exit is a combination of ammonia recycling and HCO3- flux (either via Cl-/HCO3- exchange or via a Cl- channel). Ammonia recycling involves NH4(+) uptake on the Na-K-ATPase followed by diffusive NH3 exit [S. M. Wall. Am. J. Physiol. 270 (Renal Physiol. 39): F432-F439, 1996]; model calculations suggest that this is the principal mode of base exit. By virtue of this mechanism, the model also suggests that realistic elevations in peritubular K+ concentration will compromise IMCD acid secretion. Although ammonia recycling is insensitive to carbonic anhydrase (CA) inhibition, the base exit linked to HCO3- flux provides a CA-sensitive component to acid secretion. In model simulations, it is observed that increased luminal NaCl entry increases ammonia cycling but decreases peritubular Cl-/HCO3- exchange (due to increased cell Cl-). This parallel system of peritubular base exit stabilizes acid secretion in the face of variable Na+ reabsorption.
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PMID:A mathematical model of the inner medullary collecting duct of the rat: acid/base transport. 961 22

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

The intracellular calcium ([Ca(2+)](i)) response of outer medullary descending vasa recta (OMDVR) endothelia to ANG II was examined in fura 2-loaded vessels. Abluminal ANG II (10(-8) M) caused [Ca(2+)](i) to fall in proportion to the resting [Ca(2+)](i) (r = 0. 82) of the endothelium. ANG II (10(-8) M) also inhibited both phases of the [Ca(2+)](i) response generated by bradykinin (BK, 10(-7) M), 835 +/- 201 versus 159 +/- 30 nM (peak phase) and 169 +/- 26 versus 103 +/- 14 nM (plateau phase) (means +/- SE). Luminal ANG II reduced BK (10(-7) M)-stimulated plateau [Ca(2+)](i) from 180 +/- 40 to 134 +/- 22 nM without causing vasoconstriction. Abluminal ANG II added to the bath after luminal application further reduced [Ca(2+)](i) to 113 +/- 9 nM and constricted the vessels. After thapsigargin (TG) pretreatment, ANG II (10(-8) M) caused [Ca(2+)](i) to fall from 352 +/- 149 to 105 +/- 37 nM. This effect occurred at a threshold ANG II concentration of 10(-10) M and was maximal at 10(-8) M. ANG II inhibited both the rate of Ca(2+) entry into [Ca(2+)](i)-depleted endothelia and the rate of Mn(2+) entry into [Ca(2+)](i)-replete endothelia. In contrast, ANG II raised [Ca(2+)](i) in the medullary thick ascending limb and outer medullary collecting duct, increasing [Ca(2+)](i) from baselines of 99 +/- 33 and 53 +/- 11 to peaks of 200 +/- 47 and 65 +/- 11 nM, respectively. We conclude that OMDVR endothelia are unlikely to be the source of ANG II-stimulated NO production in the medulla but that interbundle nephrons might release Ca(2+)-dependent vasodilators to modulate vasomotor tone in vascular bundles.
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PMID:Inhibition of calcium signaling in descending vasa recta endothelia by ANG II. 1074 21

Extracellular nucleotides regulate renal transport. A luminal P2Y2 receptor in mouse cortical collecting duct (CCD) principal cells has been demonstrated elsewhere. Herein the effects of adenosine triphosphate (ATP) and uridine triphosphate (UTP) on electrogenic Na+ absorption in perfused CCD of mice kept on a low-NaCl diet were investigated. Simultaneously, transepithelial voltage (V(te)), transepithelial resistance (R(te)), and fura-2 [Ca2+]i fluorescence were measured. Baseline parameters were V(te), -16.5 +/- 1.2 mV; R(te), 80.8 +/- 7.1 Omega cm2; and equivalent short-circuit current (I(sc)), -261.0 +/- 25.1 microA/cm2 (n = 45). Amiloride (10 microM) almost completely inhibited I(sc) to -3.9 +/- 3.8 microA/cm2 (n = 10). Luminal ATP (100 microM) reduced V(te) from -16.5 +/- 2.1 to -12.5 +/- 1.93 and increased R(te) from 113.1 +/- 16.2 to 123.8 +/- 16.7 Omega cm2, which resulted in a 31.7% inhibition of amiloride-sensitive I(sc) (n = 12). Similarly, luminal UTP reversibly reduced V(te) from -22.0 +/- 2.1 to -13.6 +/- 2.1 mV and increased R(te) from 48.4 +/- 5.3 to 59.2 +/- 7.1 Omega cm2, which resulted in 49.1% inhibition of Na+ absorption (n = 6). In parallel, luminal ATP and UTP elevated [Ca2+]i in CCD, increasing the fura-2 ratio by 2.7 +/- 0.7 and 4.0 +/- 1.2, respectively. Basolateral ATP and UTP (100 microM) also inhibited amiloride-sensitive I(sc) by 21.8 (n = 14) and 20.1% (n = 8), respectively. Inhibition of luminal nucleotide-induced [Ca2+]i increase by Ca2+ store depletion with cyclopiazonic acid (3 microM) did not affect nucleotide-mediated inhibition of Na+ transport (n = 7). No evidence indicated the activation of a luminal Ca2+-activated Cl- conductance, a phenomenon previously shown in M-1 CCD cells (J Physiol 524: 77-99, 2000). In essence, these data indicate that luminal ATP and UTP, most likely via P2Y2 receptors, mediate inhibition of amiloride-sensitive I(sc) in perfused mouse CCD. This inhibition appears to occurs independently of an increase of cytosolic Ca2+.
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PMID:Luminal P2Y2 receptor-mediated inhibition of Na+ absorption in isolated perfused mouse CCD. 1175 16

We studied the mechanisms of K(+) transport in cells from isolated and perfused collecting tubules and ducts from the mesonephric kidney of the toad Bufo bufo. Cells were impaled with microelectrodes across the basal cell membrane. The basolateral membrane potential (V(bl)) depolarized upon change of bath [K(+)] from 3 to 20 mmol l(-1) demonstrating a large K(+) conductance in this membrane. In collecting tubules and collecting ducts a V(bl) of -66+/-2 mV and -74+/-4 mV depolarized by 30+/-2 mV and 36+/-3 mV, respectively (N=23; 15). The K(+) channel inhibitor Ba(2+) (1 mmol l(-1)) inhibited the basolateral K(+) conductance and depolarized a V(bl) of -64+/-4 mV by 30+/-6 mV (N=8). Luminal K(+) steps (3 to 20 mmol l(-1)) demonstrated a K(+) conductance in the apical cell membrane. In collecting tubules and collecting ducts a V(bl) of -70+/-3 mV and -73+/-3 mV depolarized by 11+/-3 mV and 16+/-3 mV, respectively (N=11; 11). This conductance could also be inhibited by Ba(2+), which depolarized a V(bl) of -71+/-5 mV by 9+/-3 mV (N=5). The pump inhibitor ouabain (1 mmol l(-1)) depolarized V(bl), but addition of furosemide to bath solution did not affect V(bl). The [K(+)] in urine varied from 1.3 to 22.8 mmol l(-1). In conclusion, we propose that the collecting duct system of B. bufo secretes K(+) into the urine via luminal K(+) channels.
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PMID:K(+) transport in the mesonephric collecting duct system of the toad Bufo bufo: microelectrode recordings from isolated and perfused tubules. 1191 86

Nucleotide binding to purinergic P2 receptors contributes to the regulation of a variety of physiological functions in renal epithelial cells. Whereas P2 receptors have been functionally identified at the basolateral membrane of the cortical collecting duct (CCD), a final regulatory site of urinary Na(+), K(+), and acid-base excretion, controversy exists as to whether apical purinoceptors exist in this segment. Nor has the distribution of receptor subtypes present on the unique cell populations that constitute Ca(2+) the CCD been established. To examine this, we measured nucleotide-induced changes in intracellular Ca(2+) concentration ([Ca(2+)](i)) in fura 2-loaded rabbit CCDs microperfused in vitro. Resting [Ca(2+)](i) did not differ between principal and intercalated cells, averaging approximately 120 nM. An acute increase in tubular fluid flow rate, associated with a 20% increase in tubular diameter, led to increases in [Ca(2+)](i) in both cell types. Luminal perfusion of 100 microM UTP or ATP-gamma-S, in the absence of change in flow rate, caused a rapid and transient approximately fourfold increase in [Ca(2+)](i) in both cell types (P < 0.05). Luminal suramin, a nonspecific P2 receptor antagonist, blocked the nucleotide- but not flow-induced [Ca(2+)](i) transients. Luminal perfusion with a P2X (alpha,beta-methylene-ATP), P2X(7) (benzoyl-benzoyl-ATP), P2Y(1) (2-methylthio-ATP), or P2Y(4)/P2Y(6) (UDP) receptor agonist had no effect on [Ca(2+)](i). The nucleotide-induced [Ca(2+)](i) transients were inhibited by the inositol-1,4,5-triphosphate receptor blocker 2-aminoethoxydiphenyl borate, thapsigargin, which depletes internal Ca(2+) stores, luminal perfusion with a Ca(2+)-free perfusate, or the L-type Ca(2+) channel blocker nifedipine. These results suggest that luminal nucleotides activate apical P2Y(2) receptors in the CCD via pathways that require both internal Ca(2+) mobilization and extracellular Ca(2+) entry. The flow-induced rise in [Ca(2+)](i) is apparently not mediated by apical P2 purinergic receptor signaling.
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PMID:Effects of luminal flow and nucleotides on [Ca(2+)](i) in rabbit cortical collecting duct. 1216 94

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