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  • 11
    Electronic Resource
    Electronic Resource
    Cyclosporin-A-induced effects on the free Ca2+ concentration in LLC-PK1-cells and their mechanisms (2000)
    Springer
    Pflügers Archiv 439 (2000), S. 627-633 
    Details
    ISSN: 1432-2013
    Keywords: Ca2+ Cyclosporin A Fura-2 Kidney LLC-PK1-cells Nephrotoxicity Proximal tubule Signal transduction Tacrolimus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Here we have examined the effects of Cyclosporin A (CyA) on the free intracellular Ca2+ concentration ([Ca2+]i) of LLC-PK1/PKE20 cells to evaluate mechanisms of CyA nephrotoxicity using Fura-2 microspectrofluorometry or digital fluorescence video imaging. The CyA-associated changes were compared to the effects of tacrolimus (Tac), a structurally unrelated immunosuppressant with similar cellular pathways which also causes nephrotoxicity. CyA (EC50: 1 nmol/l, n=16) and Tac (EC50: 1 nmol/l, n=5) caused a concentration-dependent increase of [Ca2+]i which was substantially attenuated by reducing the external Ca2+ concentration (10–6 mol/l). Similarly Cyclosporin H, a non-immunosuppressive analogue of CyA, stimulated a Ca2+ influx. Nicardipine (10–6 mol/l) reduced the CyA- and the Tac-induced Ca2+ influx to 52±16% (n=10) and 13±10% (n=13) of control respectively. Diltiazem and verapamil (10–6 mol/l) were also effective, but flufenamate (10–4 mol/l), Gd3+ (10–5 mol/l) and La3+ (10–5 mol/l) were not. In the absence of extracellular Ca2+ CyA led to a small but significant [Ca2+]i increase, indicating additional release from internal stores. Depletion of inositol-1,4,5-trisphosphate- (InsP 3-) sensitive Ca2+ stores by extracellular ATP (10–4 mol/l) in low-Ca2+ solution completely suppressed the CyA-induced [Ca2+]i rise. CyA had no effect on the cellular InsP 3 concentration. Furthermore, inhibition of phospholipase-Cβ (PLCβ) by U73122 (2×10–5 mol/l) did not alter the CyA-stimulated [Ca2+]i rise. A direct effect of CyA on InsP 3-sensitive Ca2+ stores, the InsP 3 receptor, the Ca2+ content of the stores or involvement of additional stores is assumed. Incubation with CyA for 1, 12 and 24 h enhanced the rise in [Ca2+]i peak induced by ATP, arginine vasopressin (AVP) and angiotensin II. In summary, CyA stimulated a [Ca2+]i increase in LLC-PK1 cells through Ca2+ release from InsP 3-sensitive stores and Ca2+ influx via a nicardipine-sensitive pathway. The CyA-mediated [Ca2+]i increase is independent of PLCβ activity and InsP 3 metabolism. CyA caused long-term enhancement of the agonist-induced rise in [Ca2+]i. The effects of CyA on Ca2+ signaling appear to be independent of its immunosuppressive action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004249900205
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  • 12
    Electronic Resource
    Electronic Resource
    Antidiuretic hormone acts via V1 receptors on intracellular calcium in the isolated perfused rabbit cortical thick ascending limb (1991)
    Springer
    Pflügers Archiv 417 (1991), S. 622-632 
    Details
    ISSN: 1432-2013
    Keywords: ADH ; V1 receptor ; dDAVP ; Intracellular Ca2+ ; Fura-2 ; In vitro microperfusion ; Rabbit kidney ; Cortical thick ascending limb
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effect of antidiuretic hormone ([Arg]vasopressin, ADH) on intracellular calcium activity [Ca2+]i of isolated perfused rabbit cortical thick ascending limb (cTAL) segments was investigated with the calcium fluorescent dye fura-2. The fluorescence emission ratio at 500–530 nm (R) was monitored as a measure of [Ca2+]i after excitation at 335 nm and 380 nm. In addition the transepithelial potential difference (PD te) and transepithelial resistance (R te) of the tubule were measured simultaneously. After addition of ADH (1–4 nmol/l) to the basolateral side of the cTAL R increased rapidly, but transiently, from 0.84±0.05 to 1.36±0.08 (n = 46). Subsequently, within 7–12 min R fell to control values even in the continued presence of ADH. The increase in R evoked by the ADH application corresponded to a rise of [Ca2+]i from a basal level of 155±23 nmol/l [Ca2+]i up to 429±53 nmol/l [Ca2+]i at the peak of the transient, as estimated by intra- or extracellular calibration procedures. The electrical parameters (PD te and R te) of the tubules were not changed by ADH. The ADH-induced Ca2+ transient was dependent on the presence of Ca2+ on the basolateral side, whereas luminal Ca2+ had no effect. d(CH2)5[Tyr(Me)2]2,Arg8vasopressin, a V1 antagonist (Manning compound, 10 nmol/l), blocked the ADH effect on [Ca2+]i completely (n = 5). The V2 agonist 1-desamino-[d-Arg8]vasopressin (10 nmol/l, n=4), and the cAMP analogues, dibutyryl-cAMP (400 μmol/l, n = 4), 8-(4-chlorophenylthio)-cAMP (100 μmol/l, n = 1) or 8-bromo-cAMP (200 μmol/1, n = 4) had no influence on [Ca2+]i. The ADH-induced [Ca2+]i increase was not sensitive to the calcium-channel blockers nifedipine and verapamil (100 μmol/l, n = 4). We conclude that ADH acts via V1 receptors to increase cytosolic calcium activity transiently in rabbit cortical thick ascending limb segments, possibly by an initial Ca2+ release from intracellular stores and by further Ca2+ influx through Ca2+ channels in the basolateral membrane. These channels are insensitive to L-type Ca2+ channel blockers, e.g. nifedipine and verapamil.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00372961
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  • 13
    Electronic Resource
    Electronic Resource
    Vergleichende klinische und morphologische Untersuchungen zwischen einem Neugeborenen mit Hypertrichosis universalis und gleichaltrigen hautgesunden Kindern (1968)
    Springer
    European journal of pediatrics 102 (1968), S. 327-340 
    Details
    ISSN: 1432-1076
    Keywords: Hypertrichosis universalis ; Morphologie der Lanugo
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Es wird über ein Mädchen mit Hypertrichosis universalis berichtet. Es stand von der Neugeborenenzeit bis zu seinem Tode im Alter von 2 Jahren in unserer Beobachtung. Abgesehen von der Haaranomalie wurden keine Besonderheiten festgestellt. In der Ausführung wird auf die bekannten Menschen mit H.u. eingegangen. Das Leiden kommt in zwei Erscheinungsformen vor und tritt sporadisch wie familiär auf. Zahnmißbildungen sind häufig mit dem Leiden verbunden. Auf Grund der histologischen Untersuchungen der Haut — die Haarbulbi und-papillen liegen in der Subcutis und nicht, wie bei hautgesunden Kindern, im Corium — wird die Vermutung geäußert, daß diese Haare in ihrem Wachstumsrhythmus geändert sind, das heißt, daß sie im Vergleich zu den Lanugo- und Wollhaaren einen verlängerten Wachstumscyclus haben. Eine erfolgversprechende Behandlung ist nicht bekannt.
    Notes: Summary A girl with hypertrichosis universalis is described, which could be followed from the newborn period until his death at age 2 years. In addition to the abnormality of the hair no other peculiarities were noted. The so far known cases of H. u. are discussed. The disorder is seen in two manifestations and occurs sporadically and in certain families. Teeth disturbances are frequently associated with the disease. Based on histological studies of the skin — the hair bulbs and hair papilli are located in the subcutis and not as usual in the corium — the theory is advanced, that these hairs may have a different growth cycle, i.e. a prolonged one as compared with lanugo and vellus hair. A promising therapy is not known.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00436761
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  • 14
    Electronic Resource
    Electronic Resource
    Evidence for agonist-induced export of intracellular Ca2+ in epithelial cells (1993)
    Springer
    Pflügers Archiv 424 (1993), S. 423-430 
    Details
    ISSN: 1432-2013
    Keywords: [Ca2+]i export ; Thapsigargin ; fura-2 ; HT29 ; CFPAC-1 ; ATP ; Carbachol ; Neurotensin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract There is increasing evidence that some agonists not only induce intracellular Ca2+ increases, due to store release and transmembranous influx, but also that they stimulate Ca2+ efflux. We have investigated the agonist-stimulated response on the intracellular Ca2+ activity ([Ca2+]i) in the presence of thapsigargin (10−8 mol/l, TG) in HT29 and CFPAC-1 cells. For CFPAC-1 the agonists ATP (10−7–10−3 mol/l, n=9), carbachol (10−6–10−3 mol/l, n=5) and neurotensin (10−10–10−7 mol/l, n=6) all induced a concentration-dependent decrease in [Ca2+]i in the presence of TG. Similar results were obtained with HT29 cells. This decrease of [Ca2+]i could be caused by a reduced Ca2+ influx, either due to a reduced driving force for Ca2+ in the presence of depolarizing agonists or due to agonist-regulated decrease in Ca2+ permeability. Using the fura-2 Mn2+ quenching technique we demonstrated that ATP did not slow the TG-induced Mn2+ quench. This indicates that the agonist-induced [Ca2+]i decrease in the presence of TG was not due to a reduced influx of Ca2+ into the cell, but rather due to stimulation of Ca2+ export. We used the cell attached nystatin patch clamp technique in CFPAC-1 cells to examine whether, in the presence of TG, the above agonists still led to the previously described electrical changes. The cells had a mean membrane voltage of −49±3.6 mV (n=9). Within the first 3 min ATP was still able to induce a depolarization which could be attributed to an increase in Cl− conductance. This was expected, since at this time after TG stimulation all Ca2+ agonists still liberated some [Ca2+]i. When TG incubation was prolonged, agonist application led to strongly attenuated or to no electrical responses. Therefore, the agonist-stimulated [Ca2+]i decrease cannot be explained by the reduction of the driving force for Ca2+ into the cell. In the same cells hypotonic swelling (160 mosmol/l, n=15) still induced a further [Ca2+]i increase in the presence of TG and concomitantly induced Cl− and K+ conductances. We conclude that the agonist-induced decrease of [Ca2+]i in the presence of TG probably unmasks a stimulation of [Ca2+]i export.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00374904
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  • 15
    Electronic Resource
    Electronic Resource
    Cystic fibrosis transmembrane conductance regulator activates water conductance in Xenopus oocytes (1997)
    Springer
    Pflügers Archiv 434 (1997), S. 841-847 
    Details
    ISSN: 1432-2013
    Keywords: Key words wtCFTR ; Water channels ; Chloride channels ; Glibenclamide ; Xenopus oocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Multiple properties have been attributed to the cystic fibrosis transmembrane conductance regulator (CFTR), the gene product which is mutated in cystic fibrosis (CF). In this context it has been reported that CFTR transports water. In the present study we demonstrate that expression of wild-type CFTR (wtCFTR) in Xenopus oocytes and then stimulation by 3-isobutyl-1-methylxanthine (IBMX, 1 mmol/l) activates a Cl–conductance and, in parallel, a water conductance, as measured by a volume increase gravimetrically. In water-injected control oocytes or oocytes expressing a mutant form of CFTR (G551D-CFTR) IBMX had very little effect on Cl–conductance and no effect on water conductance. Phloretin (350 μmol/l) and p-chloromercuri-benzene sulphonate (pCMBS, 1 mmol/l) inhibited water transport but did not inhibit Cl–currents when measured in double-electrode voltage-clamp experiments. In contrast, glibenclamide (100 μmol/l) inhibited wtCFTR Cl–conductance but did not inhibit water conductance in IBMX-stimulated oocytes. Moreover, gravimetric and [14C]glycerol uptake measurements indicated enhanced glycerol uptake by wtCFTR-expressing oocytes after stimulation with IBMX. Enhanced glycerol uptake could be inhibited by phloretin and pCMBS but not by glibenclamide. Taken together, the data suggest that activation of wtCFTR by an increase of intracellular cAMP is paralleled by the activation of a gylcerol-permeable water conductance. Both water and Cl–conductive pathways can be inhibited differentially. Thus, water permeation through wtCFTR probably occurs at a site of CFTR which is spatially apart from the domain responsible for Cl–conductance, or CFTR might be a regulator of an endogenous water channel in oocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050473
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  • 16
    Electronic Resource
    Electronic Resource
    Effects of arylaminobenzoate-type chloride channel blockers on equivalent short-circuit current in rabbit colon (1991)
    Springer
    Pflügers Archiv 419 (1991), S. 190-196 
    Details
    ISSN: 1432-2013
    Keywords: Colon ; Rabbit ; NPPB ; Chloride channel blockers ; Chloride secretion ; Secretory diarrhoea
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Arylaminobenzoates were examined in rabbit colon mounted in an Ussing chamber. The open-circuit transepithelial voltage (V te) and resistance (R te) were measured and the equivalent short-circuit current (I SC=V te/ R te) was calculated. After serosal (s) and mucosal (m) addition of indomethacin (1 μmol/l) I SC was −71±11 (n = 118) μA/cm2. Amiloride (0.1 mmol/l, m) inhibited this current and reversed the polarity to + 32±4 (n=118) μA/cm2. In the presence of amiloride and indomethacin, prostaglandin E2 (1 μmol/l, s), known to induce Cl− secretion, generated an I SC of -143 ± 8 (n = 92) μA/cm2. The arylaminobenzoate and Cl− channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB) reduced I SC reversibly with a half-maximal inhibition (IC50) at approximately 0.35 mmol/l and 0.2 mmol/l for mucosal and serosal application respectively. To test whether the poor effect was caused by mucus covering the luminal surface, dose/response curves of the mucosal effect were repeated after several pretreatments. Acidic pH on the mucosal side reduced IC50 to approximately 0.1 mmol/l. A similar effect was observed after N-acetyl-l-cysteine (m) preincubation. Pretreatment with N-acetyl-l-cysteine (m) and carbachol (s), in order to exhaust mucus secretion, and l-homocysteine (m) were more effective and reduced IC50 to approximately 50 μmol/l. To test whether this effect of NPPB was caused by non-specific effects, the two enantiomers of 5-nitro-2-(+/−1-phenylethylamino)-benzoate were tested of which only the (+) form inhibited the Cl− conductance in the thick ascending limb of the loop of Henle (TAL). In the present study the (+) enantiomer inhibited significantly more strongly than the (−) form. This suggests that the inhibitory effect of NPPB, even though it requires rather high concentrations, is probably due to Cl− channel inhibition. For other arylaminobenzoates the sequence of potencies was different from that determined for the TAL. The present data indicate that substances that have been designed to block the Cl− conductance of the TAL segment also inhibit reversibly but with much lower affinity the PGE2-induced Cl− secretion in rabbit colon.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00373006
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  • 17
    Electronic Resource
    Electronic Resource
    The effect of intracellular pH on cytosolic Ca2+ in HT29 cells (1996)
    Springer
    Pflügers Archiv 433 (1996), S. 98-108 
    Details
    ISSN: 1432-2013
    Keywords: Key words CO2/HCO3 ; NH3/NH4+ ; pHi ; [Ca2+]i ; Fura-2 ; BCECF ; Ca2+ store ; Ca2+ influx ; Inositol 1 ; 4 ; 5-trisphosphate ; Epithelia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The influence of intracellular pH (pHi) on intracellular Ca2+ activity ([Ca2+]i) in HT29 cells was examined microspectrofluorometrically. pHi was changed by replacing phosphate buffer by the diffusible buffers CO2/HCO3 –or NH3/NH4 + (pH 7.4). CO2/HCO3 –buffers at 2,5 or 10% acidified pHi by 0.1, 0.32 and 0.38 pH units, respectively, and increased [Ca2+]i by 8–15 nmol/l. This effect was independent of the extracellular Ca2+ activity and the filling state of thapsigargin-sensitive Ca2+ stores. Removing the CO2/HCO3 –buffer alkalinized pHi by 0.14 (2%), 0.27 (5%), and 0.38 (10%) units and enhanced [Ca2+]i to a peak value of 20, 65, and 143 nmol/l, respectively. Experiments carried out with Ca2+-free solution and with thapsigargin showed that the [Ca2+]i transient was due to release from intracellular pools and stimulated Ca2+ entry. NH3/NH4 + (20 mmol/l) induced a transient intracellular alkalinization by 0.6 pHunits and increased [Ca2+]i to a peak (Δ [Ca2+]i = 164 nmol/l). The peak [Ca2+]i increase was not influenced by removal of external Ca2+, but the decline to basal [Ca2+]i was faster. Neither the phospholipase C inhibitor U73122 nor the inositol 1,4,5-trisphosphate (InsP 3) antagonist theophylline had any influence on the NH3/NH4 +-stimulated [Ca2+]i increase, whereas carbachol-induced [Ca2+]i transients were reduced by more than 80% and 30%, respectively. InsP 3 measurements showed no change of InsP 3 during exposure to NH3/NH4 +, whereas carbachol enhanced the InsP 3 concentration, and this effect was abolished by U73122. The pHi influence on ”capacitative” Ca2+ influx was also examined. An acid pHi attenuated, and an alkaline pHi enhanced, carbachol- and thapsigargin-induced [Ca2+]i influx. We conclude that: (1) an alkaline pHi releases Ca2+ from InsP 3-dependent intracellular stores; (2) the store release is InsP 3 independent and occurs via an as yet unknown mechanism; (3) the store release stimulates capacitative Ca2+ influx; (4) the capacitative Ca2+ influx activated by InsP 3 agonists is decreased by acidic and enhanced by alkaline pHi. The effects of pHi on [Ca2+]i should be of relevance under many physiological conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050254
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  • 18
    Electronic Resource
    Electronic Resource
    The cystic fibrosis transmembrane conductance regulator attenuates the endogenous Ca2+ activated Cl– conductance of Xenopus oocytes (1997)
    Springer
    Pflügers Archiv 435 (1997), S. 178-181 
    Details
    ISSN: 1432-2013
    Keywords: Key words CFTR ; Ca2+ ; Chloride channels ; Ionomycin ; Xenopus oocytes ; CF
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Oocytes from Xenopus laevis activate a Ca2+ dependent Cl– conductance when exposed to the Ca2+ ionophore ionomycin. This Ca2+ activated Cl– conductance (CaCC) is strongly outwardly rectifying and has a halide conductivity ratio (GI– / GCl–) of about 4.4. This is in contrast to the cystic fibrosis transmembrane conductance regulator (CFTR)-Cl– conductance, which produces more linear I/V curves with a GI– / GCl– ratio of about 0.52. Ionomycin enhanced CaCC (ΔG) in water injected and CFTR expressing ooyctes in the absence of 3-isobutyl-1-methylxanthine (IBMX, 1 mmol/l) by (μS) 23 ± 1.9 (n=9) and 23.6 ± 2.3 (n=11). Stimulation by IBMX did not change CaCC in water injected oocytes. CaCC was inhibited in CFTR-expressing ooyctes after stimulation with IBMX or a membrane permeable form of cAMP and was only 5.1 ± 0.48 μS (n=18) and 6.9 ± 0.6 (n=3), respectively. Inhibition of CaCC was correlated to the amount of CFTR-current activated by IBMX. ΔF508-CFTR which demonstrates only a small residual function in activating a cAMP dependent Cl– channel in oocytes inhibited CaCC to a lesser degree (ΔG=12.1 ± 1.1 μS; n=7). Changes of CFTR and CaCC-Cl– whole cell conductances were also measured when extracellular Cl– was replaced by I–. The results confirmed the reduced activation of CaCC in the presence of activated CFTR. No evidence was found for inhibition of CFTR-currents by increase of intracellular Ca2+. Moreover, intracellular cAMP was not changed by ionomycin and stimulation by IBMX did not change the ionomycin induced Ca2+ increase in Xenopus oocytes. Taken together, these results suggest that activation of CFTR-Cl– currents is paralleled by an inhibition of Ca2+ activated Cl– currents in ooyctes of Xenopus laevis. These results provide another example for CFTR-dependent regulation of membrane conductances other than cAMP-dependent Cl– conductance. They might explain previous findings in epithelial tissues of CF-knockout mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050498
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  • 19
    Electronic Resource
    Electronic Resource
    Hypertonic cell shrinkage reduces the K+ conductance of rat colonic crypts (1998)
    Springer
    Pflügers Archiv 436 (1998), S. 227-232 
    Details
    ISSN: 1432-2013
    Keywords: Key words K+ channel ; Nonselective cation channel ; Volume regulation ; Calcium ; Ca2+
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  It has previously been shown in studies of a renal epithelial cell line that nonselective cation (NSC) channels are activated by exposure to hypertonic solution. We have also found such channels in excised patches of colonic crypt cells. They require high Ca2+ activities on the cytosolic side and a low ATP concentration for their activation and have not been recorded from cell-attached patches of colonic crypts. We examine here whether this type of channel is activated by hypertonic cell shrinkage. Bath osmolality was increased by addition of 25, 50 or 100 mmol/l mannitol. Cell-attached and whole-cell patch recordings were obtained from rat base and mid-crypt cells. In whole-cell recordings we found that addition of 50 or 100 mmol/l mannitol depolarized these cells significantly from –78±2.0 to –66±3.8 mV (n=22) and from –78±1.3 to –56±2.6 mV (n=61), respectively, and reduced the whole-cell conductance from 20±8.0 to 14±6.6 nS (n=7) and from 20±3.0 to 9.8±1.6 nS (n=19), respectively. In cell-attached patches K+ channels with a single-channel conductance of ≈16 pS were found in most recordings. The activity of these channels (N×P o, N=number, P o=open channel probability) was reduced from 2.08±0.37 to 0.98±0.23 (n=15) by the addition of 50 mmol/l mannitol and from 1.75±0.26 to 0.77±0.20 (n=12) by 100 mmol/l mannitol. No NSC channel activity was apparent in any of these recordings. Previously we have shown that the 16-pS K+ channel is controlled by cytosolic Ca2+ ([Ca2+]i). Therefore we measured [Ca2+]i by the fura-2 method and found that hypertonic solution reduced [Ca2+]i significantly (n=16). These data indicate that exposure of rat colonic crypts to hypertonic solutions does not activate NSC channels; [Ca2+]i falls in hypertonic solution leading to a reduction in the value of K+ channel N×Po, a reduced whole-cell conductance and depolarization of mid-crypt cells. These processes probably assist volume regulation inasmuch as they reduce KCl losses from the cell.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050626
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  • 20
    Electronic Resource
    Electronic Resource
    Luminal ATP induces K+ secretion via a P2Y2 receptor in rat distal colonic mucosa (1998)
    Springer
    Pflügers Archiv 436 (1998), S. 712-716 
    Details
    ISSN: 1432-2013
    Keywords: Key words ATP ; Distal colon ; Exocrine secretion ; K+ secretion ; Luminal receptors ; P2Y2 receptor ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  We have previously investigated, in studies of rat distal colonic mucosa, the effect of ATP added to the basolateral side on ion transport and [Ca2+]i. It was demonstrated that ATP acts via a P2Y1 receptor to increase [Ca2+]i and NaCl secretion. In the present study we investigated the effect of luminally added nucleotides (ATP, UTP) on transepithelial voltage (V te) and resistance (R te) in Ussing chamber experiments on rat distal colonic mucosa. Both nucleotides induced a rapid and transient (within 30 s) change of V te to lumen-positive values (resting V te: –2±1 mV; peak V te after 100 µmol/l ATP: +2.4±1.1 mV) and a decrease of R te from 89.9±10.3 to 83.8±9.1 Ωcm2 (n=10). Similar values were obtained with luminal UTP (n=15). The estimated EC50 values for both nucleotides were approximately 6 µmol/l. The ATP-induced V te effect was nearly completely sensitive to Ba2+. Addition of the K+ channel blocker Ba2+ (1 mmol/l) to the luminal solution reversibly inhibited 77±4% (n=5) of the ATP-induced V te effect. Experiments to identify the respective P2 receptor subtype revealed the following rank order of potency at 500 µmol/l agonist: UTP≥ATP〉〉2-methylthio-ATP=ADP〉〉adenosine〉 AMP〉β,γ-methylene-ATP (n=5). This closely resembles the published rank order for the P2Y2 receptor. Using the reverse-transcriptase polymerase chain reaction (RT-PCR) technique P2Y2 receptor-specific mRNA was detected in total RNA extracted from isolated crypts. In summary these data indicate that luminal ATP and UTP act via a P2Y2 receptor in the luminal membrane of colonic mucosa to elicit a transient K+ secretion.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004240050693
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