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  • Electronic Resource  (18)
  • Na+ channel  (11)
  • Rat  (7)
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  • Electronic Resource  (18)
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  • 1
    Electronic Resource
    Electronic Resource
    Regulation of epithelial ion channels by the cystic fibrosis transmembrane conductance regulator (1996)
    Springer
    Journal of molecular medicine 74 (1996), S. 527-534 
    Details
    ISSN: 1432-1440
    Keywords: Cystic fibrosis ; Cl- channel ; K+ channel ; Na+ channel ; Respiratory tract ; Colon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In most epithelia ion transport is tightly regulated. One major primary target of such regulation is the modulation of ion channels. The present brief review focuses on one specific example of ion channel regulation by the cystic fibrosis transmembrane conductance regulator (CFTR). CFTR functions as a cAMP-regulated Cl- channel. Its defect leads to the variable clinical pictures of cystic fibrosis (CF), which today is understood as a primary defect of epithelial Cl- channels in a variety of tissues such as the respiratory tract, intestine, pancreas, skin, epididymis, fallopian tube, and others. Most recent findings suggest that CFTR also acts as a channel regulator. Three examples are discussed by which CFTR regulates other Cl- channels, K+ channels, and epithelial Na+ channels. From this perspective it is evident that CFTR may play a major role in the integration of cellular function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00204979
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  • 2
    Electronic Resource
    Electronic Resource
    Regulation of epithelial ion channels by the cystic fibrosis transmembrane conductance regulator (1996)
    Springer
    Journal of molecular medicine 74 (1996), S. 527-534 
    Details
    ISSN: 1432-1440
    Keywords: Key words Cystic fibrosis ; Cl ; channel ; K+ channel ; Na+ channel ; Respiratory tract ; Colon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Abstract: In most epithelia ion transport is tightly regulated. One major primary target of such regulation is the modulation of ion channels. The present brief review focuses on one specific example of ion channel regulation by the cystic fibrosis transmembrane conductance regulator (CFTR). CFTR functions as a cAMP-regulated Cl–channel. Its defect leads to the variable clinical pictures of cystic fibrosis (CF), which today is understood as a primary defect of epithelial Cl–channels in a variety of tissues such as the respiratory tract, intestine, pancreas, skin, epididymis, fallopian tube, and others. Most recent findings suggest that CFTR also acts as a channel regulator. Three examples are discussed by which CFTR regulates other Cl–channels, K+ channels, and epithelial Na+ channels. From this perspective it is evident that CFTR may play a major role in the integration of cellular function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001090050056
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  • 3
    Electronic Resource
    Electronic Resource
    Handling of allantoin by the rat kidney (1975)
    Springer
    Pflügers Archiv 357 (1975), S. 201-207 
    Details
    ISSN: 1432-2013
    Keywords: Allantoin ; Uricase ; Kidney ; Clearance ; Micropuncture ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Renal excretion of allantoin was measured by tracer techniques. After injection of 2-C14 urate and H3 inulin, clearances of allantoin and inulin were measured and both proximal and distal tubules were micropunctured. In confirmation of earlier results 2-C14 urate injected into an intact animal is very rapidly converted to C14 allantoin: after 15 min more than 90% of urinary tracer is present as allantoin. It was further observed that 1) allantoin clearance is essentially identical with inulin clearance over a wide range of urine flows; 2) no net transport of allantoin occurs in either proximal or distal tubules. Clearly allantoin is handled by the rat kidney like inulin. The total excretion of filtered allantoin unlike that of filtered urate provides an easy and effective mechanism for animals possessing the enzyme uricase to dispose of their purine loads.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00585975
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  • 4
    Electronic Resource
    Electronic Resource
    In vivo studies on uricase activity in the rat (1974)
    Springer
    Pflügers Archiv 351 (1974), S. 323-330 
    Details
    ISSN: 1432-2013
    Keywords: Uricase ; Urate ; Allantoin ; Liver ; Kidney ; Microperfusion ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. In vivo uricase activity was tested in rats by injection of 2-C14 urate and measurement of the total C14 activity and the fractional activities of allantoin, allantoic acid and urea in samples of blood and urine. In control animals, 5 min after the injection, 70% of the plasma tracer was already present in the form of allantoin. No allantoic acid and urea were produced. Intestinectomy had no measurable influence on uricase activity. On the other hand, hepatectomy or ligation of the hepatic artery combined with subtotal viscerectomy did abolish uricase activity almost completely. 2. Following microinjections into proximal tubules of Ringer solution containing 2-C14 urate, urine samples during early recovery mainly contained labelled urate, whereas in later samples the fraction of labelled allantoin increased. About 12 min after the microinjection the urine of both kidneys contained equal amounts of tracer mainly in the form of allantoin. 3. When segments of proximal tubules were perfused with an equilibrium solution containing tracer amounts of C 14 urate, no urate was metabolized during its passage through the proximal tubule. 4. C 14 urate was offered from the peritubular capillaries and samples of tubular fluid were analyzed, Again, all the tracer in the tubular fluid was in the form of urate, indicating that urate is not oxidized when it is transported across the tubular cell. It is concluded from these results that: 1. The rat kidney has no significant uricase activity. 2. Urate transport in the kidney is not influenced by this enzyme. 3. The degradation of urate to allantoin takes place at extrarenal sites, mainly in the liver.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00593318
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  • 5
    Electronic Resource
    Electronic Resource
    The ion conductances of colonic crypts from dexamethasone-treated rats (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 419-426 
    Details
    ISSN: 1432-2013
    Keywords: Colon ; Triamterene ; Amiloride ; Na+ channel ; Cl− channel ; K+ channel ; Carbachol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Whole-cell patch-clamp studies were performed in isolated colonic crypts of rats pretreated with dexamethasone (6 mg/kg subcutaneously on 3 days consecutively prior to the experiment). The cells were divided into three categories according to their position along the crypt axis: surface cells (s.c.); mid-crypt cells (m.c.) and crypt base cells (b.c.). The zero-current membrane voltage (V m) was −56 ± 2 mV in s.c (n = 34); −76 ± 2 mV in M.C. (n = 47); and −87 ± 1 mV in b.c. (n = 87). The whole-cell conductance (G m) was similar (8–12 nS) in all three types of cells. A fractional K+ conductance accounting for 29–67% ofG m was present in all cell types. A Na+conductance was demonstrable in s.c. by the hyperpolarizing effect onV m of a low-Na+ (5 mmol/1) solution. In m.c. and b.c. the hyperpolarizing effect was much smaller, albeit significant. Amiloride had a concentration-dependent hyperpolarizing effect onV m in m.c. and even more so in s.c.. It reducedG m by approximately 12%. The dissociation constant (K D) was around 0.2 μmol/l. Triamterene had a comparable but not additive effect (K D = 30 μmol/l,n = 14). Forskolin (10 μmol/l, in order to enhance cytosolic adenosine 3′, 5′-cyclic monophosphate or CAMP) depolarizedV m in all three types of cells. The strongest effect was seen in b. c..G m was enhanced significantly in b.c. by 83% (forskolin) to 121% [8-(4-chlorophenylthio)cAMP]. The depolarization ofV m and increase inG m was caused to large extent by an increase in Cl− conductance as shown by the effect of a reduction in bath Cl− concentration from 145 to 32 mmol/1. This manocuvre hyperpolarizedV m under control conditions significantly by 6–9 mV in all three types of cells, whilst it depolarizedV m in the presence of forskolin in m.c. and in b.c.. These data indicate that s.c. of dexamethasone-treated rats possess mostly a K+ conductance and an amiloride- and Tramterene-inhibitable Na+ conductance. m.c. and b.c. possess little or no Na+ conductance; theirV m is largely determined by a K+ conductance. Forskolin (via cAMP) augments the Cl− conductance of m.c. and b.c. but has only a slight effect on s.c.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02207281
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  • 6
    Electronic Resource
    Electronic Resource
    The ion conductances of colonic crypts from dexamethasone-treated rats (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 419-426 
    Details
    ISSN: 1432-2013
    Keywords: Key words Colon ; Triamterene ; Amiloride ; Na+ channel ; Cl ; channel ; K+ channel ; Carbachol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Whole-cell patch-clamp studies were performed in isolated colonic crypts of rats pretreated with dexamethasone (6 mg/kg subcutaneously on 3 days consecutively prior to the experiment). The cells were divided into three categories according to their position along the crypt axis: surface cells (s.c.); mid-crypt cells (m.c.) and crypt base cells (b.c.). The zero-current membrane voltage (V m) was −56 ± 2 mV in s.c (n = 34); −76 ± 2 mV in m.c. (n = 47); and −87 ± 1 mV in b.c. (n = 87). The whole-cell conductance (G m) was similar (8–12 nS) in all three types of cells. A fractional K+ conductance accounting for 29–67% of G m was present in all cell types. A Na+ conductance was demonstrable in s.c. by the hyperpolarizing effect on V m of a low-Na+ (5 mmol/l) solution. In m.c. and b.c. the hyperpolarizing effect was much smaller, albeit significant. Amiloride had a concentration-dependent hyperpolarizing effect on V m in m.c. and even more so in s.c.. It reduced G m by approximately 12%. The dissociation constant (K D) was around 0.2 μmol/l. Triamterene had a comparable but not additive effect (K D = 30 μmol/l, n = 14). Forskolin (10 μmol/l, in order to enhance cytosolic adenosine 3′, 5′-cyclic monophosphate or cAMP) depolarized V m in all three types of cells. The strongest effect was seen in b.c.. G m was enhanced significantly in b.c. by 83% (forskolin) to 121% [8-(4-chlorophenylthio)cAMP]. The depolarization of V m and increase in G m was caused to large extent by an increase in Cl−conductance as shown by the effect of a reduction in bath Cl−concentration from 145 to 32 mmol/l. This manoeuvre hyperpolarized V m under control conditions significantly by 6–9 mV in all three types of cells, whilst it depolarized V m in the presence of forskolin in m.c. and in b.c.. These data indicate that s.c. of dexamethasone-treated rats possess mostly a K+ conductance and an amiloride- and triamterene-inhibitable Na+ conductance. m.c. and b.c. possess little or no Na+ conductance; their V m is largely determined by a K+ conductance. Forskolin (via cAMP) augments the Cl− conductance of m.c. and b.c. but has only a slight effect on s.c.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02207281
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  • 7
    Electronic Resource
    Electronic Resource
    The amiloride inhibitable Na+ conductance of rat colonic crypt cells is suppressed by forskolin (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 984-986 
    Details
    ISSN: 1432-2013
    Keywords: Cl− secretion ; Na+ absorption ; CAMP ; exocrine secretion ; Cl− channel ; Na+ channel ; colon
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Previously we have shown that mid crypt cells of corticoid treated rats possess an amiloride inhibitable Na+ conductance (NAC) and show an increased Cl− conductance when stimulated by prostaglandin or the second messenger CAMP. The NAC is supposed to determine the magnitude of NaCl absorption. The Cl− conductance defines the magnitude of NaCl secretion. In the present whole cell (WC) patch clamp study we have examined whether the amiloride (3 μmol/l) inhibitable NAC is downregulated when the Cl− conductance is increased by forskolin (5 μmol/l, n = 20) or the phosphodiesterase inhibitor IBMX (1 mmol/l, n = 5). Under control conditions the amiloride inhibitable NAC was 2.7 ± 0.4 nS. Forskolin depolarized the voltage from -58 ± 2.0 to-48 ± 1.9 mV and enhanced the WC conductance by 3.25 ± 0.6 nS in these cells. The amiloride inhibitable NAC was reduced to 0.38 ± 0.2 nS. These data confirm that forskolin enhances the Cl− conductance in these cells and they show for the first time that the Na+ conductance is reduced simultaneously. Thus the cells are able to change the direction of NaCl transport from absorption to secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02332187
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  • 8
    Electronic Resource
    Electronic Resource
    Crypt base cells show forskolin-induced Cl− secretion but no cation inward conductance (1996)
    Springer
    Pflügers Archiv 431 (1996), S. 427-434 
    Details
    ISSN: 1432-2013
    Keywords: Key words Colon ; Loop diuretics ; Na+ channel ; Cl ; channel ; Non-selective channel ; Exocrine secretion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Whole-cell patch-clamp studies in base cells of isolated colonic crypts of rats pretreated with dexa-methasone were performed to examine the effects of stimulation by forskolin (10 μmol/l). The experiments were designed in order to distinguish between two postulated effector mechanisms: the activation of a non-selective cation channel and the activation of Cl− channels. As shown in an accompanying report, forskolin depolarizes the membrane voltage (V m) by some 40–50 mV and enhances the whole-cell membrane conductance (G m) substantially in these cells. In this report all experiments were performed in the presence of forskolin. A reduction of the bath Na+ concentration from 145 to 2 mmol/l led to a hyperpolarization of V m by some 20–30 mV. This hyperpolarization occurred very slowly suggesting that the hyperpolarization produced by the low-Na+ solution was caused indirectly and not by a change in the equilibrium potential for Na+, E Na+. A complete kinetic analysis of the effect on voltage of bath Na+ revealed a saturation-type relation with a high apparent affinity for Na+ of around 5–10 mmol/l. A reduction in bath Cl− concentration from 145 to 32 mmol/l caused a depolarization of V m from −34 ± 3 to −20 ± 4 mV (n = 13) in the presence of a high bath Na+ concentration, but had the opposite effect at low (5 mmol/l) Na+ concentrations: V m was hyperpolarized from −46 ± 4 to −62 ± 6 mV (n = 13). If the effect of Na+ on V m was caused by a non-selective cation channel the opposite would have been expected. To test directly whether the Na+2Cl−K+ cotransporter was responsible for the effects of changes in bath Na+ on V m, the effects of increasing concentrations of several loop diuretics were examined. Furosemide, piretanide, torasemide and bumetanide (up to 0.1–0.5 mmol/l) all hyperpolarized V m, albeit only by less than 10 mV. Another subclass of loop diuretics containing a tetrazolate in position 1 [e.g. azosemide, no. 19A and no. 20A from Schlatter E, Greger R, Weidtke C (1983) Pflüger Arch 396: 210–217] were much more effective. Azosemide hyperpolarized V m from −46 ± 3 to −74 ± 2 mV (n = 18) and reduced G m from 11 ± 1 to 4 ± 1 nS (n = 14). These data indicate that forskolin stimulates Cl− secretion in these cells by a mechanism fully compatible with the current scheme for exocrine secretion involving the Na+2Cl−K+ cotransporter.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02207282
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  • 9
    Electronic Resource
    Electronic Resource
    Blockade of epithelial Na+ channels by triamterenes – underlying mechanisms and molecular basis (1996)
    Springer
    Pflügers Archiv 432 (1996), S. 760-766 
    Details
    ISSN: 1432-2013
    Keywords: Key words Triamterene ; Amiloride ; Na+ channel ; Epithelia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The three subunits (α, β, γ) encoding for the rat epithelial Na+ channel (rENaC) were expressed in Xenopus oocytes, and the induced Na+ conductance was tested for its sensitivity to various triamterene derivatives. Triamterene blocked rENaC in a voltage-dependent manner, and was 100-fold less potent than amiloride at pH 7.5. At −90 mV and −40 mV, the IC50 values were 5 μM and 10 μM, respectively. The blockage by triamterene, which is a weak base with a pK a of 6.2, was dependent on the extracellular pH. The IC50 was 1 μM at pH 6.5 and only 17 μM at pH 8.5, suggesting that the protonated compound is more potent than the unprotonated one. According to a simple kinetic analysis, the apparent inhibition constants at −90 mV were 0.74 μM for the charged and 100.6 μM for the uncharged triamterene. The main metabolite of triamterene, p-hydroxytriamterene sulfuric acid ester, inhibited rENaC with an approximately twofold lower affinity. Derivatives of triamterene, in which the p-position of the phenylmoiety was substituted by acidic or basic residues, inhibited rENaC with IC50 values in the range of 0.1–20 μM. Acidic and basic triamterenes produced a rENaC blockade with a similar voltage and pH dependence as the parent compound, suggesting that the pteridinemoiety of triamterene is responsible for that characteristic. Expression of the rENaC α-subunit-deletion mutant, Δ278–283, which lacks a putative amiloride-binding site, induced a Na+ channel with a greatly reduced affinity for both triamterene and amiloride. In summary, rENaC is a molecular target for triamterene that binds to its binding site within the electrical field, preferably as a positively charged molecule in a voltage- and pH-dependent fashion. We propose that amiloride and triamterene bind to rENaC using very similar mechanisms.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050196
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  • 10
    Electronic Resource
    Electronic Resource
    Na+ and Cl− conductances in airway epithelial cells: increased Na+ conductance in cystic fibrosis (1995)
    Springer
    Pflügers Archiv 431 (1995), S. 1-9 
    Details
    ISSN: 1432-2013
    Keywords: Na+ channel ; Respiratory epithelial cells ; Human Na+ channel ; Micropuncture ; Patch clamp ; Cystic fibrosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Na+ and Cl− conductances in the apical membrane of respiratory epithelial cells are essential for electrolyte and water transport in the airways. Apart from the well described defect in adenosine 3′∶5′ cyclic monophosphate-(cAMP-) dependent activation of Cl− conductances in cystic fibrosis (CF), an increased Na+ conductance has also been reported from transepithelial measurements. In the present experiments we tried to identify these conductances in nasal epithelial cells using patch-clamp and microelectrode techniques. With these methods we found identical and relatively low membrane voltages of about −36 mV in both freshly isolated and primary cultured normal and CF nasal epithelial cells. A Cl− conductance could be activated by cAMP in normal (ΔG=3.1±0.8 nS, n=10) but not in CF (ΔG=0.3±0.1 nS, n=11) cells, whereas Ca2+-dependent Cl− currents activated by adenosine 5′-triphosphate (ATP) and bradykinin were present in both types of cells. Cell-attached membrane patches from stimulated cells did not reveal discernible singlechannel events when activated with any of the agonists. A Na+ conductance was also detected in freshly isolated ciliated respiratory cells in impalement studies, as evidenced by the hyperpolarization induced by 10 μmol/l amiloride (ΔV= −5.2±0.6 mV, n=56) and when Na+ was replaced in the bath by N-methyld-glucamine (NMDG) (ΔV = −5.7±0.9 mV, n=14). In whole-cell patch-clamp experiments, the amilorideinduced hyperpolarization was significantly larger in CF (ΔV = −9.7±2.4 mV, n=22) when compared to normal (ΔV = −3.3±0.9 mV, n=27) cells in short-term culture. Reverse transcriptase polymerase chain reaction analysis of normal respiratory cells identified messenger RNA of both the cystic fibrosis transmembrane conductance regulator (CFTR) as well as the human epithelial Na+ channel (hNaCh). The present experiments confirm the absence of a cAMP-dependent Cl− conductance in CF respiratory epithelial cells and support previous findings obtained in transepithelial and microelectrode studies which indicate an increased Na+ conductance in respiratory epithelial cells from CF patients.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374371
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