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)

Most of filtered K+ is reabsorbed passively in the proximal tubule since the tubular fluid (TF): plasma (P) concentration ratio is almost identical to the equilibrium value calculated from the transtubular potential difference. In the loop of Henle, K+ also moves passively along chemical and electrical gradients. Only 5-10% of the filtered K+ remains in the early distal convoluted tubule. In the distal convoluted tubule TF/P K+ is lower than the calculated equilibrium value suggesting that K+ is passively secreted and actively reabsorbed. Most of the excreted K+ had been secreted by the end of the distal convoluted tubule. Aldosterone increases K+ secretion in this segment, an effect that may be dissociated from the effect on Na+. The relation between K+ secretion and Na+ absorption is the consequence of the luminal electronegativity produced by Na+ absorption and is not stoichiometric. Acidosis and alkalosis decrease and increase K+ secretion in the distal tubule respectively; this is not due to reciprocal changes in H+ secretion. Normally, some K+ is reabsorbed in the collecting duct. During K+ deprivation and loading the collecting duct may participate in the conservation or elimination of K+ respectively. Adaptation to chronic K+-loading consists of renal and extrarenal factors. The extrarenal mechanism is aldosterone-dependent and consists of rapid uptake of K+ by muscle. The renal mechanism consists of increased K+ secretion by the distal tubule. Luminal electronegativity and increased K+ pool in the distal tubular cell play a crucial role.
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PMID:Disposition and regulation of body potassium: an overview. 13 35

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.
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PMID:Segmental heterogeneity of epithelial transport in rat large intestine. 56 27

To examine the pathways of K permeation in the cortical collecting duct (CCD) from K-restricted rabbits, we studied the effects of the following three maneuvers: 1) luminal amiloride addition; 2) luminal Ba addition; and 3) luminal Na removal. Luminal addition of amiloride (1 mM) significantly increased the 86Rb lumen-to-bath efflux coefficient (KRb), and this effect was fully blocked by the presence of 2 mM luminal Ba. Addition of 2 mM luminal Ba reduced KRb both in the absence of luminal Na and in the presence of luminal Na. In contrast to the effect of amiloride addition, removal of luminal Na significantly increased KRb, but neither 2 mM luminal Ba nor 4 mM luminal Ba totally abolished this effect. However, simultaneous addition of luminal Ba and Sch 28080 (10 microM) fully inhibited the increase in KRb upon luminal Na removal, indicating that luminal Na removal enhances Rb efflux in part via H-K-adenosinetriphosphatase (H-K-ATPase). To test whether Na acts as a partial agonist for cation efflux via the H-K-ATPase we examined the effect of Sch 28080 on the 22Na lumen-to-bath efflux coefficient (KNa). These studies were conducted in the presence of 0.1 mM luminal amiloride to block fully apical conductive Na efflux, and the effect of Sch 28080 on KNa was examined at two different ambient K concentrations. In the presence of 0.5 mM K, Sch 28080 (10 microM) significantly inhibited KNa from 47.6 +/- 4.8 to 35.0 +/- 6.8 nm/s (P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of rubidium permeation by rabbit cortical collecting duct during potassium restriction. 133 11

We have reported that in the rabbit cortical collecting duct (CCD) we can identify electrophysiologically three distinct cell types; the collecting duct (CD) cell and the alpha- and beta-intercalated (IC) cell. To further characterize the Cl- transport properties of each cell type, we examined the interaction between Cl- and other halogens or SCN- in the isolated and perfused CCD by intracellular microelectrode impalement. The rapid depolarization of the basolateral membrane potential (VB) caused by replacement of bath Cl- with each anion revealed that the sequences of apparent halogen selectivity for the basolateral Cl- conductance were similar in all three cell types. The ranking of Cl- > Br- > F- > I- corresponds to the sequence 5 of Eisenman's series, indicating "strong" interaction of the anions with the selectivity site. The basolateral Cl- conductance of these three cell types may share common characteristics, although I- permeability is less in IC cells than in CD cells. Hyperpolarization of the basolateral membrane of the beta-IC cell upon reduction of luminal Cl- reflects alterations in either Cl- entry across the apical membrane, or Cl- exit across the basolateral membrane, or both. Luminal Cl- replacement with each anion showed that the sequence of the hyperpolarization of the basolateral membrane was I- >> cyclamate = SCN- > F- > Br-, suggesting that I-inhibits either apical Cl- entry or basolateral Cl- exit. On the other hand, in the CD cell reduction of the perfusate Cl- by replacement with each anion caused the basolateral membrane to hyperpolarize with a different ranking: cyclamate = F- > I- = SCN- > Br-.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interaction of Cl- and other halogens with Cl- transport systems in rabbit cortical collecting duct. 144 75

Arginine vasopressin (AVP) transiently stimulates Na+ transport in the rabbit cortical collecting duct (CCD). However, the sustained effect of both AVP and its putative second messenger, cyclic adenosine monophosphate (cAMP), on Na+ transport in the rabbit CCD is inhibitory. Because maneuvers that increase [Ca++]i inhibit Na+ transport, the effects of AVP and cell-permeable cAMP analogues, on [Ca++]i were investigated in fura-2-loaded in vitro microperfused rabbit CCDs. Low-dose AVP (23-230 pM) selectively stimulated Ca++ influx, whereas 23 nM AVP additionally released calcium from intracellular stores. 8-chlorophenylthio-cAMP (8CPTcAMP) and 8-bromo-cAMP (8-Br-cAMP) also increased CCD [Ca++]i. The 8CPTcAMP-stimulated [Ca++]i increase was totally dependent on basolateral [Ca++]. In the absence of cAMP, peritubular Na+ removal produced a marked increase in [Ca++]i, which was also dependent on bath [Ca++], suggesting the existence of basolateral Na+/Ca++ exchange. Luminal Na+ removal in the absence of cAMP did not alter CCD [Ca++]i, but it completely blocked the cAMP-stimulated [Ca++]i increase. Thus the cAMP-dependent Ca++ increase is totally dependent on both luminal Na+ and basolateral Ca++, suggesting the [Ca++]i increase is secondary to cAMP effects on luminal Na+ entry and its coupling to basolateral Na+/Ca++ exchange. 8CPTcAMP inhibits lumen-to-bath 22Na flux [JNa(l-b)] in CCDs bathed in a normal Ca++ bath (2.4 mM). However, when bath Ca++ was lowered to 100 nM, a maneuver that also blocks the 8CPTcAMP [Ca++]i increase, 8CPTcAMP stimulated, rather than inhibited JNa(l-b). These results suggest that cAMP formation initially stimulates CCD Na+ transport, and that increased apical Na+ entry secondarily activates basolateral Ca++ entry. The cAMP-dependent [Ca++]i increase leads to inhibition Na+ transport in the rabbit CCD.
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PMID:Feedback inhibition of cyclic adenosine monophosphate-stimulated Na+ transport in the rabbit cortical collecting duct via Na(+)-dependent basolateral Ca++ entry. 165 41

To examine the exact target cell and mechanism of action of epidermal growth factor (EGF) in the isolated cortical collecting duct from rabbit kidney, we compared electrical properties of collecting duct (CD) cells (principal cells) and intercalated (IC) cells in absence and presence of EGF at 10(-8) M. Differentiation of CD and IC cells was based on values of basolateral membrane voltage (Vb) and fractional apical membrane resistance (fRa). In CD cells, upon addition of EGF to bath, lumen-negative transepithelial voltage (VT) was decreased from -8.0 +/- 1.9 to -2.4 +/- 1.3 mV (n = 22, P less than 0.001), but Vb was little changed (from -85.1 +/- 2.8 to -83.1 +/- 2.7 mV, n = 19), indicating that EGF in bath mainly caused changes in apical membrane voltage. In addition, peritubular EGF increased transepithelial resistance (RT) from 132.9 +/- 15.8 to 153.8 +/- 18.4 omega.cm2 (n = 16, P less than 0.001) as well as fRa from 0.31 +/- 0.06 to 0.39 +/- 0.07 (n = 12, P less than 0.01). These actions of EGF were prevented by pretreatment with 50 microM luminal amiloride. Luminal EGF had no effects on VT, Vb, RT, or fRa of CD cells. In IC cells, upon addition of EGF to bath, neither Vb nor fRa was affected. From these results, we conclude that EGF acts on the CD cell at the basolateral border and inhibits mainly the amiloride-sensitive Na+ conductance in the apical membrane.
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PMID:Site and mechanism of action of epidermal growth factor in rabbit cortical collecting duct. 199 68

To examine mechanisms of H+ extrusion in the inner stripe of outer medullary collecting duct (OMCDIS), cell pH (pHi) was measured microfluorometrically in in vitro perfused tubules by use of 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. In total absence of luminal and peritubular Na+, pHi recovery from an acid load (NH3/NH+4 pulse) occurred at an initial rate of 0.13 +/- 0.02 pH units/min, whereas in the presence of 135 mM peritubular Na+, pHi recovered at 1.40 +/- 0.28 pH units/min. Na(+)-dependent pHi recovery was completely inhibited by 1.0 mM peritubular amiloride. Luminal Na+ (135 mM) addition had no effect on pHi recovery. Na(+)-independent pHi recovery from acid load was manifest by a triphasic response: 1) initial slow alkalinization; 2) slow cell acidification; and 3) a final phase that exhibited gradually increasing rates of alkalinization, returning pHi above the initial control level (pre-NH3/NH+4 pulse). Luminal N-ethylmaleimide (NEM, 500 microM), an H(+)-ATPase inhibitor, significantly inhibited initial rate of pHi recovery and total pHi recovery; whereas 500 microM peritubular NEM had no effect on initial rate of pHi recovery. Luminal SCH 28080 (100 microM), an H(+)-K(+)-ATPase inhibitor, had no effect on initial rate of pHi recovery or total pHi recovery. Thus rabbit OMCDIS possesses both an apical membrane NEM-sensitive, SCH 28080-insensitive, Na(+)-independent H+ extrusion mechanism (likely a simple H(+)-translocating ATPase) and a basolateral membrane amiloride-sensitive Na(+)-H+ antiporter.
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PMID:Apical and basolateral membrane H+ extrusion mechanisms in inner stripe of rabbit outer medullary collecting duct. 217 59

The effect of parathyroid hormone (PTH) on ion transport was examined by observing transmural (VT) and basolateral membrane voltage (VB) in the in vitro perfused rabbit connecting tubule. Addition of 10 nmol/l PTH to the bath induced a biphasic response of VT, with hyperpolarization followed by depolarization. Chlorophenylthioadenosine cyclic 3',5'-monophosphate mimicked the effect of PTH, which did not change the VB in the connecting tubule cell, but mainly caused changes in the apical membrane voltage. The VT of distal convoluted tubule and the cortical collecting duct were not affected by PTH. Elimination of Na+ from the lumen abolished the PTH-induced VT responses in the connecting tubule. In the presence of 10 mumol/l amiloride, PTH caused an initial hyperpolarization but did not induce the late depolarization. The same was seen in the absence of luminal Ca2+. Either addition of 0.1 mmol/l ouabain to the bath or elimination of bath Na+ completely abolished the PTH-induced VT changes. The presence of 5 mmol/l Ba2+ in the lumen did not affect the response to PTH. These findings indicate that the initial hyperpolarization may be caused by an increase in Na+ influx across the luminal membrane through an amiloride-insensitive Na+ conductive pathway and that the late depolarization may be caused by the decrease in Na+ influx through the amiloride-sensitive Na+ conductive pathway. Luminal Ca2+ is necessary for the late depolarization caused by PTH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of parathyroid hormone on the connecting tubule from the rabbit kidney: biphasic response of transmural voltage. 238 63

To determine the exact site and mechanism of action of thiazide diuretics, effects of 10(-4) M trichlormethiazide (TCM) on NaCl transport were examined in the distal convoluted tubule (DCT), the connecting tubule (CNT) and the cortical collecting duct (CCD) of rabbit kidney by the in vitro microperfusion technique. TCM added to the lumen decreased lumen-to-bath 36Cl flux (JCl(LB)) only in the CNT without changing the transmural voltage (VT). In the DCT, 10(-4) M furosemide did not change JCl(LB) even if it was added to the lumen with 10(-4) M TCM, whereas 10(-5) M amiloride in the lumen decreased the lumen-to-bath 22Na flux (JNa(LB)) and VT. In the CNT, TCM added to the lumen did not affect the bath-to-lumen 36Cl flux. Addition of TCM to the bath slightly decreased JCl(LB). Luminal addition of 10(-4) M TCM also decreased JNa(LB). Amiloride at 10(-5) M in the lumen decreased both JNa(LB) and VT. Addition of TCM with 10(-5) M amiloride further decreased JNa(LB) without affecting VT, indicating that TCM affects the electroneutral Na+ transport, which is distinct from the amiloride-sensitive conductive Na+ pathway. When Na+ was removed from the lumen, JCl(LB) was markedly decreased, but addition of TCM did not cause further decrease in JCl(LB). Furosemide did not affect JCl(LB), but addition of both 10(-4) M TCM and furosemide decreased JCl(LB), indicating that Na+-K+-2Cl- cotransport is not involved in the action of TCM. Removal of HCO3- slightly decreased JCl(LB), and TCM caused further decrease in JCl(LB). Amiloride at 10(-3) M, a concentration supposed to inhibit the Na+/H+ antiport, slightly decreased JCl(LB), and addition of TCM caused a further marked decrease in JJl(LB). The similar results were also obtained when the combined effects of 10(-3) M 4,4'-diisothiocyano-stilben-2,2'-disulfonate(DIDS) and 10(-4) M TCM were examined. These findings suggest that the parallel antiport of Na+/H+ and Cl-/HCO3- is not involved in the action of TCM. By excluding other possible mechanisms involving neutral Na+-dependent Cl- transport, we conclude that TCM inhibits Na+-Cl- cotransport in the luminal membrane of the rabbit CNT.
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PMID:Site and mechanism of action of trichlormethiazide in rabbit distal nephron segments perfused in vitro. 284 60

Intracellular microelectrode techniques were used together with inhibitors of Na+ transport (amiloride) and H+ transport (acetazolamide and SITS) to identify principal cells and intercalated cells in the outer stripe of the rabbit outer medullary collecting duct. The principal cell (n = 9) had a basolateral membrane voltage (Vbl) of -64.7 +/- 3.2 mV, a fractional resistance of the apical membrane (fRa = Ra/Ra + Rbl) of 0.82 +/- 0.02, and a K+-selective basolateral membrane. Luminal amiloride hyperpolarized Vbl by 10.3 +/- 2.1 mV and increased fRa to near unity (n = 7). Bath acetazolamide and SITS were without effect on these parameters. The intercalated cell (n = 5) had a Vbl of -25.0 +/- 3.2 mV, a fRa of 0.99 +/- 0.01, and a Cl(-)-selective basolateral membrane. Bath acetazolamide or SITS hyperpolarized Vbl by 26.4 +/- 8.2 mV. Luminal amiloride did not alter Vbl of this cell. The differential effects of the inhibitors also indicate that the principal and intercalated cells are probably not directly coupled electrically.
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PMID:Electrophysiological identification of principal and intercalated cells in the rabbit outer medullary collecting duct. 303 50

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