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  • Electronic Resource  (18)
  • Carbachol  (11)
  • Rat  (7)
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  • Electronic Resource  (18)
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  • 1
    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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  • 2
    Electronic Resource
    Electronic Resource
    Small-conductance Cl− channels in HT29 cells: activation by Ca2+, hypotonic cell swelling and 8-Br-cGMP (1992)
    Springer
    Pflügers Archiv 421 (1992), S. 238-246 
    Details
    ISSN: 1432-2013
    Keywords: Cl− channels ; HT29 cells ; Ca2+-mobilizing hormones ; ATP ; Carbachol ; Neurotensin ; NPPB ; Patch clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study demonstrates the activation of Cl− channels in HT29 cells by agonist (ATP, neurotensin, carbachol) increasing cytosolic Ca2+, by hypotonic cell swelling and by cGMP. Cell-attached nystatin patch-clamp (CAN) as well as slow and fast wholecell recordings were used. The cell membrane potential was depolarized in a dose-dependent manner with halfmaximal effects at 0.4 umol/l for ATP, 60 pmol/l for neurotensin and 0.8 μmol/l for carbachol. The depolarization, which was caused by Cl− conductances increases, occurred within 1 s and was accompanied by a simultaneous and reversible increase of the input conductance of the cell-attached membrane from 295±32 pS to 1180±271 pS (ATP; 10 μmol/l, n=21) and 192±37 pS to 443±128 pS (neurotensin; 1 nmol/l, n=8). The effects of the agonists could be mimicked by ionomycin (0.2 umol/l), suggesting that an increase in intracellular Ca2+ was responsible for the activation of Cl− channels. The depolarization was followed by a secondary hyperpolarization. Hypotonic cell swelling also depolarized the cells and induced an increase in the membrane conductance. With 120 mmol/l NaCl the depolarization was 10±0.8 mV and the cell-attached conductance increased from 228±29 pS to 410±65 (n=26) pS. NaCl at 90 mmol/l and 72.5 mmol/l had even stronger effects. Comparable conductance increases were also obtained when the different agonists or hypotonic cell swelling were examined in whole cell experiments. 5-Nitro-2-(3-phenylpropylamino)-benzoate (1 μmol/l) did not prevent the effects of Ca2+-increasing hormones and of hypotonic solutions. An increase in Cl− conductance was also induced by 8-Br-cGMP (1 mmol/l) but not by heat-stable Escherichia coli toxin. In contrast to their conductance-increasing effects in CAN patches, the different agonists and cell swelling did not activate resolvable single channels in these cell-attached membranes. This indicates that the Cl− channels involved have a single-channel conductance too small (≤ 4 pS, 150 Hz) to be resolved by our techniques.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374833
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  • 3
    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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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    Effect of intracellular pH on agonist-induced [Ca2+]i transients in HT29 cells (1997)
    Springer
    Pflügers Archiv 434 (1997), S. 466-474 
    Details
    ISSN: 1432-2013
    Keywords: Key words BCECF ; Fura-2 ; pHi ; [Ca2+]i ; HT29 ; Carbachol ; Neurotensin ; ATP ; InsP3 ; Cell volume ; Calcein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  In this study we examined the influence of intracellular pH (pHi) on agonist-induced changes of intracellular Ca2+ activity ([Ca2+]i) in HT29 cells. pHi and [Ca2+]i were measured microspectrofluorimetrically using BCECF and fura-2, respectively. Buffers containing trimethylamine (TriMA), NH3/NH4 + and acetate were used to clamp pHi to defined values. The magnitudes of the peak and plateau of [Ca2+]i transients induced by carbachol (CCH, 10–6 mol/l) were greatly enhanced by an acidic pHi and nearly abolished by an alkaline pHi. The relationship between pHi and the [Ca2+]i peak was nearly linear from pHi 7.0 to 7.8. This effect of pHi was also observed at higher CCH concentrations (10–4 and 10–5 mol/l), at which the inhibitory effect of an alkaline pHi was more pronounced than the stimulatory effect of an acidic pHi. An acidic pHi shifted the CCH concentration/response curve to the left, whereas an alkaline pHi led to a rightward shift. The influence of pHi on [Ca2+]i transients induced by neurotensin (10–8 mol/l) or ATP (5 × 10–7 mol/l) was similar to its influence on those induced by CCH, but generally not as pronounced. Measurements of cellular inositol 1,4,5-trisphosphate (InsP 3) showed no changes in response to acidification with acetate (20 mmol/l) or alkalinization with TriMA (20 mmol/l). The InsP 3 increase induced by CCH was unaltered at an acidic pHi, but was augmented at an alkaline pHi. Confocal measurements of cell volume showed no significant changes induced by TriMA or acetate. Slow-whole-cell patch-clamp experiments showed no additional effect of CCH on the membrane voltage (V m) measured after TriMA or acetate application. We conclude that pHi is a physiological modulator of hormonal effects in HT29 cells, as the [Ca2+]i responses to agonists were significantly changed at already slightly altered pHi. The measurements of InsP 3, cell volume and V m show that pHi must act distally to the InsP 3 production, and not via changes of cell volume or V m.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050422
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  • 6
    Electronic Resource
    Electronic Resource
    Urate handling by the rat kidney (1974)
    Springer
    Pflügers Archiv 352 (1974), S. 115-120 
    Details
    ISSN: 1432-2013
    Keywords: Urate ; Reabsorption ; Loop of Henle ; Micropuncture ; Microperfusion ; Microinjection ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Reabsorption rates for urate in the loops of Henle were measured in superficial nephrons in the rat 1. under conditions of free flow, 2. using microperfusion and 3. by a microinjection technique. 1. Under conditions of free flow distally measured TF/PUA/TF/PIn-values varied between 0.51 and 0.38 in antidiuretic rats, depending on TF/PIn (UA = both uric acid and urate, In = inulin, TF/P = concentration in tubular fluid to plasma concentration). The corresponding values in samples from end-proximal tubules were 1.06 and in urine 0.19 (U/PUA/U/PIn). 2. In microperfusion experiments of Henle loops early distal recoveries of 2-C14 urate varied between 57 and 86%, depending on the flow rates (10–40 nl/min). 3. In microinjection experiments C14 recovery in urine was about 85% when tracer solution was microinjected into endproximal tubules. From these results we conclude: 1. The main site of urate reabsorption is located in the loops of Henle. 2. This reabsorption is highly dependent on flow rates. Increase of flow rate through Henle's loop decreases urate reabsorption.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00587510
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  • 7
    Electronic Resource
    Electronic Resource
    Urate interaction with plasma proteins and erythrocytes (1974)
    Springer
    Pflügers Archiv 352 (1974), S. 121-133 
    Details
    ISSN: 1432-2013
    Keywords: Urate ; Protein Interaction ; Uptake by Erythrocytes ; Renal Reabsorption ; Man ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Interaction of urate with human and rat plasma was studied by a dialysis technique at different temperatures. At 4° C a certain fraction of urate is bound to proteins. However, this fraction diminishes with increasing temperature and at 37° C only some 7–8% (in man) and 2% (in rat) interact with proteins. The finding that urate is almost completely filtered in the glomerulus is discussed. In body areas exposed to low temperatures protein binding of urate may be of importance. Urate uptake by erythrocytes is characterized by two components: a fast component equilibrating almost immediately at about 7% in man and 17% in rat and a slow component reaching equilibrium after 60 min, at 28% and 36%, respectively. The process is described by a mathematical formula. Lowering of the temperature mainly diminishes uptake by the slow component withQ 10-values ranging between 1.5 and 4.0. In the observed range of concentrations the uptake process does not saturate. The results at lower pH-values suggest that it is unionized uric acid which is transported by the slow component. Application of the data to kidney medulla supports the hypothesis that erythrocytes and, probably, to a lesser extent plasma proteins serve as vehicles for urate reabsorption in the countercurrent system. Such a temporary interaction enables uric acid to escape recirculation and to leave the kidney medulla.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00587511
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  • 8
    Electronic Resource
    Electronic Resource
    Ion conductances of isolated cortical collecting duct cells (1992)
    Springer
    Pflügers Archiv 421 (1992), S. 381-387 
    Details
    ISSN: 1432-2013
    Keywords: Rat ; Cell isolation ; K+ channels ; Na+-conductance ; Patch clamp ; Cell-attached-nystatin technique
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The study of ion conductances in the intact cortical collecting duct (CCD) with the patch-clamp method is rather difficult. An optimized method to isolate CCD cells from rat kidneys using an in vivo followed by an in vitro enzyme digestion is described. Individual CCD segments were collected after this digestion and incubated in EGTA-buffered medium. This procedure resulted in single cells or cell clusters. These freshly isolated CCD cells were studied with different modifications of the patch-clamp method. Membrane voltages measured in the cell-attached-nystatin configuration were −74 ±1mV (n=13) and −68±3 mV (n=22) in cells isolated from normal and mineralocorticoid-treated rats respectively. These values and those measured with the nystatin-perforated slow-whole-cell configuration (−79 ±1mV, n=23) are comparable to those measured in principal cells of isolated CCD segments. The cells hyperpolarized after the addition of amiloride and depolarized with the addition of adiuretin to the bath. The amiloride effect was enhanced when cells were isolated from deoxycorticosterone-acetate-treated rats. The cells were strongly depolarized upon elevation of the extracellular K+-concentration and did not demonstrate a measurable Cl− conductance. A large-conductance K+ channel (174 pS, n=5, cell-attached, 145 mmol/l K+ in the pipette; 140 pS, n=12, cell-free, 3.6 mmol/l K+ in the bath) was seen. It had a very low activity on the cell, but a high open probability when excised into a solution with 1 mmol/l Ca2+ on the cytosolic side. More often a small-conductance K+ channel (36–52 pS, n=19, cell-attached; 30 pS, n=5, cell-free) with a high open probability was found on the cell. These freshly isolated cells seem to be a powerful preparation to study the properties and regulation of ion conductances of rat CCD with several electrophysiological methods. These freshly isolated CCD cells maintain the conductance properties known from principal cells of the intact CCD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374227
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  • 9
    Electronic Resource
    Electronic Resource
    Agonist-induced intracellular Ca2+ transients in HT29 cells (1993)
    Springer
    Pflügers Archiv 423 (1993), S. 519-526 
    Details
    ISSN: 1432-2013
    Keywords: Carbachol ; Adenosine triphosphate ; Neurotensin ; Fura-2 ; Intracellular Ca2+ ; Ca2+ influx ; Mn2+ ; Verapamil ; Ni2+
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the present study we have investigated the mechanism of intracellular Ca2+ activity ([Ca2+]i) changes in HT29 cells induced by adenosine triphosphate (ATP), carbachol (CCH), and neurotensin (NT). [Ca2+]i was measured with the fluorescent Ca2+ indicator fura-2 at the single-cell level or in small cell plaques with high time resolution (1–40Hz). ATP and CCH induced not only a dose-dependent [Ca2+]i peak response, but also changes of the plateau phase. The [Ca2+]i plateau was inversely dependent on the ATP concentration, whereas the CCH-induced [Ca2+]i plateau increased at higher CCH concentrations. NT showed (from 10−10 to 10−7 mol/l) in most cases only a [Ca2+]i spike lasting 2–3 min. The [Ca2+]i plateau induced by ATP (10−6 mol/l) and CCH (10−5 mol/l) was abolished by reducing the Ca2+ activity in the bath from 10−3 to 10−4 mol/l (n=7). In Ca2+-free bathing solution the [Ca2+]i peak value for all three agonists was not altered. Using fura-2 quenching by Mn2+ as an indicator of Ca2+ influx the [Ca2+]i peak was always reached before Mn2+ influx started. Every agonist showed this delayed stimulation of the Ca2+ influx with a lag time of 23±1.5 s (n=15) indicating a similar mechanism in each case. Verapamil (10−6–10−4 mol/l) blocked dose dependently both phases (peak and plateau) of the CCH-induced [Ca2+]i increase. Short pre-incubation with verapamil augmented the effect on the [Ca2+]i peak, whereas no further influence on the plateau was observed. Ni2+ (10−3 mol/l) reduced the plateau value by 70%.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374950
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  • 10
    Electronic Resource
    Electronic Resource
    8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate (TMB-8) acts as a muscarinic receptor antagonist in the epithelial cell line HT29 (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 353 (1996), S. 295-301 
    Details
    ISSN: 1432-1912
    Keywords: Key words TMB-8 ; Fura-2 ; HT29 ; M3-receptor ; ATP ; Carbachol ; Neurotensin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  8-(N, N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) is a widely used pharmacological tool to investigate the involvement of intracellular Ca2+ stores in cellular responses. In this study we investigate the effect of TMB-8 as a putative inhibitor of “Ca2+ signalling” in single fura-2 loaded HT29 colonic epithelial cells stimulated by ATP, carbachol (CCH) and neurotensin (NT). TMB-8 effectively inhibited the CCH-induced (100 μmol/l intracellular Ca2+ ([Ca2+]i) transient with an IC50 of 20 μmol/l. However, [Ca2+]i transients induced by other phospholipase C coupled agonists ATP (10 μmol/l, n=4) and NT (10 nmol/l, n=4) remained unaffected by TMB-8 (50 μmol/l). The agonist-induced [Ca2+]i transients remained equally unaffected by 100 μmol/l TMB-8 when the stimulatory concentration was reduced to 0.5 μmol/l for ATP (n=4) or 1 nmol/l for NT (n=4). The competitive nature of the TMB-8-induced inhibition of the CCH-induced [Ca2+]i transient was demonstrated by examining the agonist at various concentrations in absence and presence of the antagonist. High TMB-8 concentrations (100 μmol/l) alone induced a small [Ca2+]i increase (Δ[Ca2+]i: 40±5 nmol/l, n=7). We assume that this increase is a consequence of a TMB-8 induced intracellular alkalinization (ΔpH: 0.1±0.02, n=7) occurring simultaneously with the increase in [Ca2+]i. From these results we draw the following conclusions: (1) In sharp contrast to a large number of other studies, but in agreement with studies in other types of cells, these results substantially challenge the value of the “tool” TMB-8 as an “intracellular Ca2+ antagonist”; (2) TMB-8 acts a muscarinic receptor antagonist at the M3 receptor; (3) TMB-8 does not influence the release of Ca2+ from intracellular stores when IP3 signal transduction is activated by ATP or NT; (4) TMB-8 as a weak organic base alkalinizes the cytosol at high concentrations; and (5) TMB-8 induces small [Ca2+]i transients at higher concentrations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168631
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