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)

Net K+ secretion is not detected in cortical collecting ducts (CCDs) isolated from newborn rabbits and perfused in vitro. To establish whether a low apical K+ permeability of the neonatal principal cell limits K+ secretion early in life, we used the patch-clamp technique in split-open CCDs isolated from maturing rabbits to study the properties and density of conducting K+ channels in principal cells. With KCl in the pipette and a NaCl solution warmed to 37 degrees C in the bath, inward currents with a conductance of approximately 42 pS were observed in 0% (0 out of 13 or 0/13), 10% (2/21), 18% (5/28), 29% (4/14), and 56% (10/18) of cell-attached patches obtained in 1-, 2-, 3-, 4-, and 5-wk-old animals, respectively. The conductance and reversal potential of this channel led us to suspect that it represented the low-conductance K+ channel previously described in the rat CCD by L. G. Palmer, L. Antonian, and G. Frindt (J. Gen. Physiol. 104: 693-710, 1994). The mean number of open channels per patch (NPo) increased progressively (P < 0.05) after birth, from 0 at 1 wk, to 0.06 +/- 0.04 at 2 wk, to 0.40 +/- 0.18 at 3 wk, to 0.74 +/- 0.41 at 4 wk, and to 1.06 +/- 0.28 at 5 wk. The increase in NPo appeared to be due primarily to a developmental increase in N, which is the number of channels; open probability, Po, remained constant at approximately 0.5 for all channels identified after the 2nd wk of life. The increase in number of conducting K+ channels during postnatal life is likely to contribute to the maturational increase in net K+ secretion in the CCDs.
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PMID:Apical K+ conductance in maturing rabbit principal cell. 908 84

The connecting tubule (CNT) contains alpha-(H(+)-secreting) and beta-(HCO(-)(3)-secreting) intercalated cells and is therefore likely to contribute to acid-base homeostasis. To characterize the mechanisms of HCO(-)(3) transport in the rabbit CNT, in which there is little definitive data presently available, we microdissected the segments from the superficial cortical labyrinth, perfused them in vitro, measured net HCO(-)(3) transport (J(HCO(-)(3))) by microcalorimetry, and examined the effects of several experimental maneuvers. Mean +/- SE basal J(HCO(-)(3)) was -3.4 +/- 0.1 pmol. min(-1). mm(-1) (net HCO(-)(3) secretion), and transepithelial voltage was -13 +/- 1 mV (n = 47). Net HCO(-)(3) secretion was markedly inhibited by removal of luminal Cl(-) or application of basolateral H(+)-ATPase inhibitors (bafilomycin or concanamycin), maneuvers that inhibit beta-intercalated cell function. Net HCO(-)(3) secretion was not affected by inhibitors of alpha-intercalated cell function (basolateral Cl(-) removal, basolateral DIDS, or luminal H(+)-ATPase inhibitors). Net HCO(-)(3) secretion was stimulated by isoproterenol and inhibited by acetazolamide. These data indicate that 1) CNTs secrete HCO(-)(3) via an apical DIDS-insensitive Cl(-)/HCO(-)(3) exchanger, mediated by a basolateral bafilomycin- and concanamycin-sensitive H(+)-ATPase; 2) inhibition of cytosolic carbonic anhydrase decreases HCO(-)(3) secretion; and 3) stimulation of beta-adrenergic receptors increases HCO(-)(3) secretion. The failure to influence net HCO(-)(3) transport by inhibiting alpha-intercalated cell apical H(+)-ATPases or basolateral Cl(-)/HCO(-)(3) exchange suggests that the CNT has fewer functioning alpha-intercalated cells than the cortical collecting duct. These are the first studies to examine the rate and mechanisms of HCO(-)(3) secretion by the rabbit CNT; this is clearly an important segment in mediating acid-base homeostasis.
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PMID:Mechanisms of HCO(-)(3) secretion in the rabbit connecting segment. 1051 81

K+ secretion by the cortical collecting duct (CCD) is stimulated at high flow rates. Patch-clamp analysis has identified a small-conductance secretory K+ (SK) and a high-conductance Ca(2+)-activated K+ (maxi-K) channel in the apical membrane of the CCD. The SK channel, encoded by ROMK, is believed to mediate baseline K+ secretion. The role of the stretch- and Ca2+-activated maxi-K channel is still uncertain. The purpose of this study was to identify the K+ channel mediating flow-dependent K+ secretion in the CCD. Segments isolated from New Zealand White rabbits were microperfused in the absence and presence of luminal tetraethylammonium (TEA) or charybdotoxin, both inhibitors of maxi-K but not SK channels, or apamin, an inhibitor of small-conductance maxi-K+ channels. Net K+ secretion and Na+ absorption were measured at varying flow rates. In the absence of TEA, net K+ secretion increased from 8.3 +/- 1.0 to 23.4 +/- 4.7 pmol. min(-1). mm(-1) (P < 0.03) as the tubular flow rate was increased from 0.5 to 6 nl. min(-1). mm(-1). Flow stimulation of net K+ secretion was blocked by luminal TEA (8.2 +/- 1.2 vs. 9.9 +/- 2.7 pmol. min(-1). mm(-1) at 0.6 and 6 nl. min(-1). mm(-1) flow rates, respectively) or charybdotoxin (6.8 +/- 1.6 vs. 8.3 +/- 1.6 pmol. min(-1). mm(-1) at 1 and 4 nl. min(-1). mm(-1) flow rates, respectively) but not by apamin. These results suggest that flow-dependent K+ secretion is mediated by a maxi-K channel, whereas baseline K+ secretion occurs through a TEA- and charybdotoxin-insensitive SK (ROMK) channel.
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PMID:Flow-dependent K+ secretion in the cortical collecting duct is mediated by a maxi-K channel. 1129 20

The recently cloned, non-erythrocyte Rh glycoproteins (Rhbg and Rhcg) are expressed in the intercalated cells of the renal collecting duct. The apical Rhcg and the basolateral Rhbg are likely involved in NH3 and/or NH4+ transport, yet the characteristics of this transport are not yet certain. In this study we investigated the mechanism of NH4+ transport by Rhbg and Rhcg expressed in Xenopus oocytes. We used a two-electrode voltage-clamp and ion-selective microelectrodes to measure NH4+-induced currents (I(NH4)) and changes in pHi, respectively. In oocytes expressing Rhcg, exposure to bath [NH4+] of 2.5-20 mM induced inward currents that were slightly more than those in H2O-injected (control) oocytes. I-V plots in the presence of NH4+ showed a small increase in slope conductance only at positive potentials. On the other hand, in oocytes expressing Rhbg, 5 mM NH4+ induced an inward I(NH4) of -79 nA, decreased pHi (DeltapHi) by 0.13 at a rate (dpHi/dt) of -2 7 x 10(-4) pH/s and depolarized the cell by 45 mV. These changes were significantly more than those in control oocytes. I-V plots in the presence of NH4+ showed substantial increase in conductance. Amiloride (1 mM) inhibited I(NH4), DeltapHi and dpHi/dt in oocytes expressing Rhbg but not in control oocytes. Raising bath [NH4+] in increments from 1 to 20 mM elicited a faster dpHi/dt, a larger decrease in pHi and a larger depolarization. Net NH4+ flux by Rhbg (estimated from dpHi/dt) was proportional to [NH4+] gradient and followed saturation kinetics with an apparent Km of 2.3 mM. Methyl ammonium (5 mM) induced a current of -63 nA in Rhbg oocytes but did not cause any change in control oocytes. These data indicate that: 1) Rhbg transport of NH4+ is electrogenic. 2) Methyl ammonium is transported by Rhbg. 3) NH4+ transport by Rhbg is saturated at high concentrations with Michaelis-Menten kinetics.
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PMID:Electrogenic ammonium transport by renal Rhbg. 1658 Aug 64

Although colonic lumen NH(4)(+) levels are high, 15-44 mM normal range in humans, relatively few studies have addressed the transport mechanisms for NH(4)(+). More extensive studies have elucidated the transport of NH(4)(+) in the kidney collecting duct, which involves a number of transporter processes also present in the distal colon. Similar to NH(4)(+) secretion in the renal collecting duct, we show that the distal colon secretory model, T84 cell line, has the capacity to secrete NH(4)(+) and maintain an apical-to-basolateral NH(4)(+) gradient. NH(4)(+) transport in the secretory direction was supported by basolateral NH(4)(+) loading on NKCC1, Na(+)-K(+)-ATPase, and the NH(4)(+) transporter, RhBG. NH(4)(+) was transported on NKCC1 in T84 cells nearly as well as K(+) as determined by bumetanide-sensitive (86)Rb-uptake. (86)Rb-uptake and ouabain-sensitive current measurement indicated that NH(4)(+) is transported by Na(+)-K(+)-ATPase in these cells to an equal extent as K(+). T84 cells expressed mRNA for the basolateral NH(4)(+) transporter RhBG and the apical NH(4)(+) transporter RhCG. Net NH(4)(+) transport in the secretory direction determined by (14)C-methylammonium (MA) uptake and flux occurred in T84 cells suggesting functional RhG protein activity. The occurrence of NH(4)(+) transport in the secretory direction within a colonic crypt cell model likely serves to minimize net absorption of NH(4)(+) because of surface cell NH(4)(+) absorption. These findings suggest that we rethink the present limited understanding of NH(4)(+) handling by the distal colon as being due solely to passive absorption.
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PMID:Ammonium transport in the colonic crypt cell line, T84: role for Rhesus glycoproteins and NKCC1. 1803 81

Stimulation of the basolateral Na(+)/K(+)-ATPase in the isolated perfused rabbit cortical collecting duct by raising either bath potassium or lumen sodium increases potassium secretion, sodium absorption and their apical conductances. Here we determined the effect of stimulating Na(+)/K(+)-ATPase on potassium secretion without luminal sodium transport. Acutely raising bath potassium concentrations from 2.5 to 8.5 mM, without luminal sodium, depolarized the basolateral membrane and transepithelial voltages while increasing the transepithelial, basolateral and apical membrane conductances of principal cells. Fractional apical membrane resistance and cell pH were elevated. Net potassium secretion was maintained albeit diminished and was still enhanced by raising bath potassium, but was reduced by basolateral ethylisopropylamiloride, an inhibitor of Na(+)/H(+) exchange. Luminal iberitoxin, a specific inhibitor of the calcium-activated big-conductance potassium (BK) channel, impaired potassium secretion both in the presence and absence of luminal sodium. In contrast, iberitoxin did not affect luminal sodium transport. We conclude that basolateral Na(+)/H(+) exchange in the cortical collecting duct plays an important role in maintaining potassium secretion during compromised sodium supplies and that BK channels contribute to potassium secretion.
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PMID:Basolateral Na+/H+ exchange maintains potassium secretion during diminished sodium transport in the rabbit cortical collecting duct. 1876 67


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