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PubMed2006

Overlapping pharmacology of Ca2+-activated Cl- and K+ channels.

Research into Ca2+-activated Cl- channels is hampered by the inability to decipher their molecular identity and the fact that all extant Cl- channel blockers have effects on other ion channels. Most notably, Cl- channel blockers such as the fenamates (e.g. niflumic acid and flufenamic acid) activate Ca2+-dependent K+ channels, although other pharmacological overlaps have been discovered. In this article, we highlight the complex pharmacology of Ca2+-activated Cl- channels and the caveats associated with using these blockers--a necessary requirement because many researchers use Cl- channel blockers as probes for Cl- channel activity. Moreover, we discuss the argument for a common structural motif between Ca2+-activated Cl- channels and Ca2+-dependent K+ channels, which has led to the possibility that the molecular identity of Cl- channels will be revealed by research in this new direction, in addition to the use of existing candidates such as the CLCA, Bestrophin and tweety genes.

Animals↗

PubMed1995

Side-effects of drugs used in the treatment of rheumatoid arthritis.

A number of anti-inflammatory and other drugs used in the treatment of rheumatoid arthritis have been screened for their ability to cause oxidative damage to lipids and proteins in vitro. Although many drugs exhibited an antioxidant profile, a few drugs tested were pro-oxidant, increasing peroxidation of arachidonic acid by mixtures of haem proteins and H2O2. This system may be an appropriate model to use in the inflammatory situation, since microbleeding to release haemoglobin occurs in the inflamed rheumatoid joint, where H2O2 is produced by invading neutrophils. The damaging effects of the pro-oxidant drugs phenylbutazone, meclofenamic acid and flufenamic acid were investigated in some detail using this system. Arachidonic acid peroxidation was accentuated in a dose-dependent manner and in the presence of haem proteins and H2O2, phenylbutazone also causes inactivation of alpha 1-antiproteinase, a major serine proteinase inhibitor in biological fluids. The above drugs may interact with ferryl haemoglobin, produced by the reaction of H2O2 with haemoglobin, to generate drug-derived radicals causing oxidative damage in these systems. If such reactions occur in vivo, they could contribute to the side-effects induced by these drugs on administration to certain rheumatoid arthritis patients.

Adrenal Cortex Hormones↗

PubMed2007

Depolarization evoked by acetylcholine in mesenteric arteries of hypertensive rats attenuates endothelium-dependent hyperpolarizing factor.

OBJECTIVE: During blockade of endothelium-dependent hyperpolarizing factor (EDHF), acetylcholine evoked larger and faster depolarization in mesenteric arteries of spontaneously hypertensive rats (SHR) than normotensive Wistar-Kyoto (WKY) rats. We studied the mechanism underlying this response and its role in the attenuation of EDHF. METHODS: Electrophysiology, computational modelling and myography were used to study changes in membrane potential and effects on contractility. RESULTS: The large acetylcholine-evoked depolarization in SHR was accompanied by contraction, but this was not seen in WKY rats. The depolarization depended on release of intracellular Ca2+ but was unaffected by nonselective cation channel inhibitors, gadolinium, lanthanum or amiloride. The depolarization was significantly reduced by the Ca2+-dependent Cl- channel inhibitors, niflumic acid or flufenamic acid, or alterations in Cl- gradients using bumetanide (Na/K/Cl transporter inhibitor) or external Cl- replacement with isethionate. These drugs altered the time course of EDHF-evoked hyperpolarizations in SHR, making them indistinguishable from those in WKY rats. EDHF-induced relaxation was less sensitive to acetylcholine in SHR than in WKY rats, but this difference was eliminated following artery pretreatment with bumetanide. Computational modelling in which the SHR fast depolarizing response was selectively modulated mimicked physiologically acquired results obtained in SHR and WKY rats during Cl- -channel blockade. CONCLUSIONS: Acetylcholine evokes a fast depolarization in SHR but not in WKY rats, mediated by the opening of Ca2+-dependent Cl- channels. The depolarization is responsible for a constriction that reduces EDHF-mediated relaxation. Data suggest that Ca2+-dependent Cl- channels may provide a novel therapeutic target for improvement of endothelial dysfunction during hypertension.

Acetylcholine↗

PubMed1995

Lysophosphatidic acid, serum, and hyposmolarity activate Cl- currents in corneal keratocytes.

The influence of serum, lysophosphatidic acid (LPA), and hyposmotic stress on the ion channel activity of normal and cryo-injured rabbit corneal keratocytes was investigated. Whole cell currents were examined using the amphotericin perforated-patch technique. In cells from wounded corneas, fetal bovine serum activated large, holding voltage-insensitive, fast-activating, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS)-, flufenamic acid-, and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB)-blockable outward currents showing inactivation at depolarized voltages. LPA activated identical currents, also only in cells from wounded corneas. Blocker and reversal potential experiments characterized the current as a Cl- currents (Icl). Lysophosphatidylcholine (10 microM) failed to activate the current. An identical current was activated by hyposmotic stimulation in cells from control and wounded corneas. Hyposmotic stimulation also activated Icl in cells from wounded corneas that were unresponsive to LPA. We conclude that serum, LPA, and hypotonic stress activate Icl in keratocytes from wounded corneas. We also conclude that LPA is a serum factor that can activate Icl and that hyposmotic activation may work through a signaling pathway separate from that of LPA.

Animals↗

PubMed1977

[Studies of sulfhemoglobin formation by various drugs (3) (author's transl)].

Sulfhemoglobin (SHb) and methemoglobin (MHb) formations by various compounds were examined by single and three consecutive intraperitoneal administrations to mice. With a single administration, methemoglobinemia was induced by diphenylamine (DPA), 1-naphthylamine (NA), phenylnaphthylamine (PNA), N-(1-naphthyl) anthranilic acid (N1) and N-(1'-naphthyl)-2-aminophenylacetic acid (IG240), and was not observed with phenylanthranilic acid (PAA), N-benzoyl-N'-phenyl-2, 6-diaminobenzoic acid (BPAA), flufenamic acid (FA), mefenamic acid (MFA), N-(2-6-dichlorophenyl) anthranilic acid (CPAA), N-(2', 6'-dichlorophenyl)-2-aminophenylacetic acid (CPPA), nine derivatives of N1 and two derivatives of IG240. On the other hand, sulfhemoglobinemia, with a single administration, was found to be induced by NA. Furthermore, with three consecutive administrations, such was induced by DPA, PAA, BPAA and FA even though SHb was not demonstrated with a single administration, and was not observed with MF, CPAA, CPPA and various derivatives of N1 and IG240.

1-Naphthylamine↗

PubMed2006

Comparison of bovine udder skin with human and porcine skin in percutaneous permeation experiments.

Rat and pig animal skin has been the most common replacement material for human skin for use in in vitro permeability experiments. Unfortunately, the permeability barrier of skin from laboratory animals is known to be relatively weak, due to significant follicular transport. Pig skin has been shown to be a suitable model for human skin. Unfortunately, it cannot be gathered from the regular slaughtering process, which makes it unsuitable for permeation experiments. We therefore studied the suitability of bovine udder skin, an untreated waste material of the butchering process, as a possible replacement material for use in in vitro permeability tests. We investigated the barrier strength of bovine udder skin against four different substances, and its histology and lipid profile, in comparison with pig skin and heat separated human epidermis. Pig and human skin were found to be equally permeable, whilst bovine udder skin seemed to exhibit a weaker, but less variable, barrier against caffeine, benzoic acid, testosterone, and flufenamic acid. The skin of all three species contained variable contents of the major lipid classes: cholesterol, ceramides, cholesterol ester, fatty acids and triglycerides. Morphological differences mainly comprised variations in the density of hair follicles. Based on these results, the amount of free fatty acids and triglycerides and the density of hair follicles seem to be important factors in the differences between the skin barriers in the three species.

Animals↗

PubMed1977

Concentrations of acidic antiinflammatory drugs in gastric mucosa.

In rats, the concentrations of the acidic antiinflammatory drugs salicylic acid, acetylsalicylic acid, phenylbutazone, flufenamic acid and indomethacin in the glandular portion of the gastric mucosa were determined 30 and 60 min after oral or subcutaneous administration. In another series of experiments, solutions of the drugs were introduced into the ligated stomach and the concentrations in the mucosa and in the contents of the stomach were determined after 60 min. The ratio between the concentrations in the musoca and those in serum or gastric contents were much lower than expected according to the distribution by passive non-ionic diffusion. This apparent discrepancy may be explained as a result of a drug-induced damage to the mucosal cell allowing free diffusion of ionized drug across the cell membrane.

Animals↗

PubMed1995

[Iontophoresis in the treatment of pain].

UNLABELLED: The objective has been to verify the effectiveness of iontophoresis in alleviating conditions of pain by means of a computer-assisted search of the pertinent literature. The search was performed with the aid of the Medline database (1984 bis 1993) and reference lists (studies from 1954). SELECTION CRITERIA: all clinical trials performed with at least one control group as well as all experimental studies conducted within the same period. The selection criteria were met by 10 experimental and 15 clinical studies. The studies were categorized by substance group. The following groups of substances were applied (experimentally/clinically): local anaesthetics (0/6), non steroidal anti-inflammatory drugs (2/3), vinca-alkaloids (1/2), corticosteroids (3/1), morphine (0/1), iodide (4/1) and fluoride (0/1). Both short-term effects (lidocaine, procaine, flufenamic acid, morphine) and long-term effects (benzocaine-salicylamide, diclofenac, Mobilat, vinca-alkaloids, dexamethasone-lidocaine, iodide, fluoride) were studied. Comparisons were made against placebo iontophoresis (lidocaine, procaine, flufenamic acid, diclofenac, Mobilat, vinca-alkaloids, dexamethasone-lidocaine, morphine, fluoride), solely topical administration (procaine, benzocaine-salicylamide, flufenamic acid), placebo administration without current (procaine, flufenamic acid), and other methods (lidocaine, iodide). With one single exception (lidocaine), none of the studies included groups without treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗

PubMed1981

[Studies on metabolism and elimination of etofenamate by dogs (author's transl)].

Renal elimination of etofenamate was studied after oral (200--1200 mg/kg) and intravenous (75 mg/kg) application to dogs. Free flufenamic acid and total fenamates (except phenolic metabolites) were determined. In accordance with other N-arylanthranilic acid derivatives after etofenamate only small amounts are renally eliminated; these results are specific for dog and differ to other animal species. Renally eliminated amounts (up to 8%) are not dependent on dose, the i.v. results also being in the same range. Proportions of free flufenamic acid is small in comparison to total fenamates. Renal elimination occurs preferentially on the first day after application. Biliary elimination of etofenamate and its metabolites was investigated after intravenous as well as intragastric application. Intact etofenamate was found after i.v. and i.g. application, part of it being conjugated. Hydroxyderivatives of Etofenamate (eto) were identified: 5-OH-eto (i.v. and i.g.), 4'-OH-eto (i.v.) and the 5.4'-dihydroxy-eto (i.g.). A further eto-derivative found after i.v. application could not be characterized. Amounts of flufenamic acid (flu) and its hydroxyderivatives (esp. 5-OH-flu) were increased after hydrolytic degradation. These results show that metabolic degradation does not occur primarily be conversion to flufenamic acid; etofenamate itself is degraded by hydroxylation and/or conjugation and subsequent formation of the corresponding flufenamic derivatives.

Animals↗

PubMed1998

A basolateral chloride conductance in rat lingual epithelium.

We used Ussing chamber measurements and whole-cell recordings to characterize a chloride conductance in rat lingual epithelium. Niflumic acid (NFA) and flufenamic acid (FFA), nonsteroidal anti-inflammatory aromatic compounds known to inhibit Cl- conductances in other tissues, reduced transepithelial short-circuit current (Isc) in the intact dorsal anterior rat tongue epithelium when added from the serosal side, and reduced whole-cell currents in rat fungiform taste cells. In both Ussing chamber and patch-clamp experiments, the effect of NFA was mimicked by replacement of bath Cl- with methanesulfonate or gluconate. In low Cl- bath solution, the effect of NFA on whole-cell current was reduced. Replacement of bath Ca2+ with Ba2+ reduced the whole-cell Cl- current. We conclude that a Ca2+-activated Cl- conductance is likely present in the basolateral membrane of the rat lingual epithelium, and is present in the taste receptor cells from fungiform papillae. Further experiments will be required to identify the role of this conductance in taste transduction.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1992

The induction of ornithine decarboxylase in human epidermis is independent of lipoxygenase and cyclo-oxygenase pathways.

In vivo studies in rodents suggest that prostaglandins and/or leukotrienes are involved in the epidermal induction of ornithine decarboxylase (ODC). Recently, we have shown that, in human epidermis, prostaglandins are not involved in this process. Here we report the role of leukotrienes in epidermal ODC induction in human skin. Topical flufenamic acid (Dignodolin), vehicle, or nothing was applied under plastic occlusion to three sites on the backs of healthy volunteers. This was followed 1 h later by Sellotape stripping. After renewed application and occlusion for 8 h, biopsies were carried out for the estimation of ODC levels. There were no significant differences in the levels of ODC between the flufenamic acid treated and control sites. To confirm this finding, test sites were irradiated with 3 MED of UVB. This was immediately followed by the application of flufenamic acid, vehicle, or nothing to the three irradiated sites. After 8 h, biopsies were taken, and the levels of ODC were again similar in the flufenamic acid- and the vehicle-treated sites. The data indicate that, following Sellotape stripping or UVB irradiation, neither lipoxygenase not cyclooxygenase products contribute to the in vivo induction of ODC in human epidermis.

Adult↗

PubMed1976

Differential effects of prostaglandin synthetase inhibitors on prostaglandin E2 binding and on prostaglandin- or cholera toxin-induced cyclic AMP accumulation in the rabbit uterus.

Cyclic 3',5'-nucleotide phosphodiesterase (PDE) activity in rabbit uterine homogenate was inhibited by indomethacin (10 mug/ml; 66% inhibition) or flufenamic and (10 mug/ml; 60%). Indomethacin (100 mug/ml) reduced uterine prostaglandin E2 (PGE2) content by 80%, but potentiated the stimulatory action of purified cholera toxin (choleragen; 800%) and of exogenous PGE2 (140%) on cyclic AMP accumulation, probably through its inhibitory effect on cyclic AMP destruction. These findings suggest that endogenous PGE2 is not an essential mediator of choleragen action. By contrast, flufenamic acid abolished choleragen and PGE2 action on cyclic AMP production. Unlabeled PGE2 (10 mug/ml), flufenamic acid, indomethacin, and aspirin (100 mug/ml each) inhibited [3H]PGE2 binding to uterine slices by 78, 73, 62, and 20% respectively. It is concluded that while indomethacin and flufenamic acid have similar effects on prostaglandin biosynthesis and PDE activity, only fenamates have an inhibitory effect on the biological action of exogenous PGE2 and choleragen on the stimulation of cyclic AMP production, probably through the inhibition of the binding of PGE2 and choleragen to its specific receptor sites. The diverse biochemical actions of the above drugs indicate that care has to be taken when using these drugs in analyzing the physiopathological roles of prostaglandins.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1993

Evidence for a role for the cyclic adenosine 3',5'-monophosphate/protein kinase-A pathway in regulation of the gonadotropin subunit messenger ribonucleic acids.

cAMP regulation of gonadotropin secretion and subunit mRNA levels was studied in pituitary cells perifused with pulses of GnRH. Pituitary cells from 7-week-old male rats castrated at 5 weeks of age were stimulated hourly for 9-24 h with 1-min pulses of GnRH, the adenylate cyclase activator forskolin, the cell-permeable cAMP analog 8-bromo-cAMP (8Br-cAMP), or control medium. Cells were also treated with the nonsteroidal antiinflammatory drug flufenamic acid, which reduces pituitary cAMP levels. During perifusion, the effluent was collected in 10-min fractions for FSH and LH assay. At the completion of perifusion, total RNA was extracted, and gonadotropin subunit mRNA levels were quantitated by Northern analysis. Continuous administration of flufenamic acid gradually reduced the amplitude of GnRH-stimulated FSH and LH pulses to nadir values of 40 +/- 4.7% and 62 +/- 12% of the control value, respectively. Flufenamic acid decreased (P < 0.05) FSH beta and alpha-subunit mRNA levels and blocked the effect of GnRH to lengthen LH beta mRNA. Pulses of forskolin or 8Br-cAMP released LH and FSH, and continuous forskolin or 8Br-cAMP potentiated the gonadotropin stimulatory effect of GnRH. Forskolin or 8Br-cAMP increased (P < 0.05) FSH beta mRNA and alpha-subunit mRNA levels when administered in pulses, but not when administered continuously, and lengthened LH beta mRNA. The Nal-Glu GnRH antagonist blocked the effects of GnRH pulses, but not the effects of 8Br-cAMP or forskolin. In conclusion, lowering intracellular cAMP levels with flufenamic acid attenuated GnRH-stimulated gonadotropin secretion, decreased alpha-subunit and FSH beta mRNA levels, and blocked the effect of GnRH to lengthen LH beta mRNA, whereas 8Br-cAMP or forskolin produced the opposite effect. These data extend previous results which suggested that cAMP modulates gonadotropin secretion and indicate that the cAMP/A-kinase pathway regulates each of the gonadotropin subunit mRNAs.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1993

Pharmacological characterization of muscarinic receptor-activated cation channels in guinea-pig ileum.

1. The pharmacological properties of cationic currents activated by acetylcholine (ACh) (Icat) in guinea-pig ileal smooth muscle cells were investigated, with conventional single patch electrode or nystatin-perforated whole-cell recording. Cs-aspartate was used as the internal solution to allow selective measurement of Icat. 2. Well-known K channel blockers, tetraethylammonium (TEA), 4-aminopyridine (4-AP), procaine and quinine as well as a Ca releasing agent, caffeine, all produced concentration-dependent inhibition of Icat with rapid onset (time constant approximately 100 ms), when applied externally. The recovery from the inhibition on washout also occurred rapidly in the order of 100 ms except in the case of quinine. Approximate values of the half inhibitory concentrations (IC50) were 10 nM for TEA and caffeine, 1-5 mM for 4-AP and procaine, and 1 microM for quinine. The mode of inhibition was voltage-dependent, i.e., depolarization relieved the inhibition with no change in reversal potential. 3. Externally applied diphenylamine-2-carboxylate (DPC) derivatives, DCDPC and flufenamic acid, produced potent inhibition of Icat at micromolar concentrations (IC50s were < 30 microM for DCDPC and 32 microM for flufenamic acid). The onset of and recovery from inhibition occurred slowly and the degree of inhibition depended on the membrane potential only weakly, without any discernible change in the reversal potential. 4. All of the above-tested drugs exhibited comparable inhibitory actions on the voltage-dependent Ca current in the concentration ranges effective at inhibiting Icat. However, amongst them, quinine and flufenamic acid seemed to have several-fold better selectivity for the Icat channel than for the voltage-dependent Ca channel. 5. Internally dialysed GTPgammaS (100 microM) induced inward cationic currents. The effects of drugs on these currents were similar to their effects on the Icat current.6. These results clearly indicate that many drugs used as pharmacological tools in smooth muscle research exert considerable nonspecific effects on various types of channels. The mechanism of inhibition and the relevance to use of these drugs as blockers for the I cat channel are discussed.

4-Aminopyridine↗

PubMed2000

Two opposing effects of non-steroidal anti-inflammatory drugs on the expression of the inducible cyclooxygenase. Mediation through different signaling pathways.

The efficacy of non-steroidal anti-inflammatory drugs (NSAIDs) is considered to be a result of their inhibitory effect on cyclooxygenase (COX) activity. Here, we report that flufenamic acid shows two opposing effects on COX-2 expression; it induces COX-2 expression in the colon cancer cell line (HT-29) and macrophage cell line (RAW 264.7); conversely, it inhibits tumor necrosis factor alpha (TNFalpha)- or lipopolysaccharide (LPS)-induced COX-2 expression. This inhibition correlates with the suppression of TNFalpha- or LPS-induced NFkappaB activation by flufenamic acid. The inhibitor of extracellular signal-regulated protein kinase, p38, or NFkappaB does not affect the NSAID-induced COX-2 expression. These results suggest that the NSAID-induced COX-2 expression is not mediated through activation of NFkappaB and mitogen-activated protein kinases. An activator of peroxisome proliferator-activated receptor gamma, 15-deoxy-Delta(12,14)-prostaglandin J(2), also induces COX-2 expression and inhibits TNFalpha-induced NFkappaB activation and COX-2 expression. Flufenamic acid and 15-deoxy-Delta(12,14)-prostaglandin J(2) also inhibit LPS-induced expression of inducible form of nitric-oxide synthase and interleukin-1alpha in RAW 264.7 cells. Together, these results indicate that the NSAIDs inhibit mitogen-induced COX-2 expression while they induce COX-2 expression. Furthermore, the results suggest that the anti-inflammatory effects of flufenamic acid and some other NSAIDs are due to their inhibitory action on the mitogen-induced expression of COX-2 and downstream markers of inflammation in addition to their inhibitory effect on COX enzyme activity.

Adenocarcinoma↗

PubMed1997

K+ and Cl- contribute to resting membrane conductance of cultured porcine endocardial endothelial cells.

The conventional whole cell patch-clamp technique was used to measure the resting membrane conductance and membrane currents of single, nonstimulated, cultured endocardial endothelial cells of the porcine right ventricle in different ionic conditions. All cells displayed the barium-sensitive, inwardly rectifying potassium (K+) current (I(Ki)). In 65% of the cells, I(Ki) was the predominant membrane current. The mean zero-current potential (V0) was -61.0 +/- 12.5 mV (+/- SD, n = 45). In 35% of the cells, I(Ki) was superposed on an outwardly rectifying (OR) current. V0 of these cells was more depolarized (-33.5 +/- 22.0 mV, n = 26). High intracellular Cl- (122 instead of 52 mmol/l) activated or increased the OR current and shifted V0 in the direction of the equilibrium potential for Cl-. In cells displaying the OR current, V0 was dependent on extracellular Cl-, indicating the contribution of an OR Cl- current in setting V0. At low intracellular Cl- (6 instead of 52 mmol/l), the OR current was decreased and V0 shifted in the direction of the equilibrium potential for K+. In cells not displaying the OR current, V0 was dependent on extracellular K+ but not on Cl-, indicating major permeability to K+ in these conditions. Block of the OR current by the Cl(-)-channel blockers anthracene-9-carboxylic acid (1 mmol/l), flufenamic acid (100-500 micromol/l), and Zn2+ (100-200 micromol/l) provided further evidence for the anionic nature of the OR current. After inhibition of I(Ki) and the OR Cl- current, a third current component was observed in 50% of the cells. The pharmacology and voltage dependence of this current suggested the presence of Ca2+-activated K+ channels in endocardial endothelial cells. We concluded that the resting membrane conductance of nonstimulated endocardial endothelial cells is mainly determined by the combined activity of inwardly rectifying K+, OR Cl-, and Ca2+-activated K+ channels.

Animals↗

PubMed1999

Delayed contact hypersensitivity to non-steroidal anti-inflammatory drugs.

Several non-steroidal anti-inflammatory drugs (NSAIDs) are available for topical treatment of acute soft tissue trauma or degenerative musculoskeletal disorders; the NSAID bufexamac is mainly used for therapy of chronic inflammatory skin diseases. In order to assess the occurrence of contact allergy to NSAIDs in 371 consecutive patients presenting for diagnosis of presumed contact allergy, patch tests were performed with a standard series and additionally with a series of NSAIDs, comprising acetylsalicylic acid, bufexamac, diclofenac, etofenamate, felbinac, flufenamic acid, ibuprofen, indomethacin, and piroxicam. 17 individuals (4.6%) exhibited delayed hypersensitivity to one of the NSAID preparations: 12 patients (3.2%) had patch test reactions to bufexamac, 2 (0.5%) to etofenamate, 2 (0.5%) to indomethacin, and 1 patient (0.3%) to flufenamic acid. These patch test results corresponded well to the individual history in 11 individuals (including 10 patients with reactions to bufexamac), and in 2 patients the clinical relevance of the reactions was probable. In view of the high frequency of allergic contact reactions to bufexamac, we propose to test this drug particularly in patients with atopic eczema or other chronic eczematous diseases.

Adolescent↗

PubMed1998

Properties of whole-cell ionic currents in cultured human corneal epithelial cells.

PURPOSE: To identify and partially characterize the ionic currents contributing to the whole-cell conductance of cultured human corneal epithelial cells. METHODS: Epithelial cells were scraped from human donor corneas and cultured for use in patch-clamp experiments. Amphotericin B and the perforated-patch configuration were used to measure whole-cell currents in cells isolated from confluent monolayers. RESULTS: Cell monolayers exhibited cobblestone morphology and were immunopositive for corneal epithelium-specific cytokeratin. Single cells had a capacitance of 21 +/- 2 pF and expressed similar types of ionic currents regardless of passage number. In descending order of frequency of occurrence, cells exhibited a nonselective cation current active at depolarized voltages and insensitive to Ba2+ and Gd3+; an outwardly rectifying K+ current active at depolarized voltages, stimulated by flufenamic acid and inhibited by tetraethylammonium; a voltage-gated inward Na+ current; an outwardly rectifying K+ current active at hyperpolarized voltages, stimulated by flufenamic acid, blocked by Ba2+, and insensitive to diltiazem; an inwardly rectifying K+ current; and a nonselective cation current inhibited by flufenamic acid. CONCLUSIONS: Our results are consistent with those in previous studies of noncultured epithelia from rabbit and human corneas showing an outwardly rectifying K+ current active at hyperpolarized voltages and a nonselective cation current active at depolarized voltages and insensitive to Ba2+. These data suggest cultured cells may be useful in determining the physiological role of ion channels in corneal epithelia and may aid in the development of a cell-based model for the examination of the effects of wounding and toxic agents on the human cornea.

Amphotericin B↗