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PubMed2002

Dietary fecal tagging as a cleansing method before CT colonography: initial results polyp detection and patient acceptance.

PURPOSE: To compare reduced colonic cleansing based on dietary fecal tagging (FT) with standard (non-FT) colonic cleansing with regard to patient acceptance, sensitivity, and specificity. MATERIALS AND METHODS: In 50 patients (FT group), FT was performed by means of diet, magnesium citrate, and a barium suspension. In another 50 patients (non-FT group), preparation was based on polyethylene glycol administration. All patients underwent conventional colonoscopy after computed tomographic (CT) colonography. Sensitivity and specificity for polyp detection were calculated by using conventional colonography as the reference standard. At CT colonography, fecal residue was evaluated. Patients were interviewed to determine discomfort, side effects, sleep quality, final opinion on examination comfort, and whether they would be reluctant to undergo the same examination again. RESULTS: FT left more fecal residue but improved differentiation from polyps (FT specificity, 88% [30 of 34 patients]; non-FT, 77% [23 of 30 patients]). Sensitivities were comparable: FT, 88% (14 of 16 patients); non-FT, 85% (17 of 20 patients). FT significantly reduced discomfort, side effects, and sleep disturbance, and resulted in an improved final opinion of how comfortable the examination was (P <.05). Although FT improved patient willingness to repeat the examination, this improvement was not statistically significant (P >.05). CONCLUSION: FT offers the patient a well-tolerated preparation and improves specificity, with improved differentiation of polyps from residual stool.

Administration, Oral↗
PubMed1988

Activation of a calcium-permeable cation channel by insulin-like growth factor II in BALB/c 3T3 cells.

Insulin-like growth factor II (IGF II) is a member of somatomedin family and is a potent mitogen in various types of mammalian cells. We have recently reported that IGF II stimulates calcium influx in competent BALB/c 3T3 cells primed with epidermal growth factor (J. Biol. Chem. 262: 12120-12126, 1987). Using patch-clamp technique, we show here an IGF II-sensitive cation channel in BALB/c 3T3 cell plasma membrane. Calcium is permeable to this cation channel and its opening behavior is independent of membrane potential. IGF II increases the opening probability of the identical channel in cells pretreated sequentially with platelet-derived growth factor and epidermal growth factor, whereas IGF II does not affect the opening of the channel in G0-arrested cells. This cation channel activity is observed only when IGF II is included in the patch pipette, indicating direct regulation of the channel by IGF II. We suggest that IGF II stimulates calcium influx by opening this cation channel and that IGF II activates the channel in a unique cell cycle-dependent manner.

Animals↗
PubMed1989

Mechanism of chloride uptake in rabbit corneal epithelium.

The mechanism of chloride uptake at the basal membrane (stromal side) of rabbit corneal epithelium was examined by observing the effects of ion transport inhibitors and ion concentrations on the stimulated epithelial short-circuit current (Isc). Loop diuretics inhibited the theophylline-stimulated peak and sustained Isc. Treatment with 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS, 0.2 mM) and/or 5-(N,N-dimethyl)amiloride (0.1 mM) as well as the potent anion exchange inhibitor, 5c(+)[(2,3,9,9a-tetrahydro-1H-fluoren-7-yl)oxy]acetic acid (0.01 mM), had no significant effect on Isc. These results are consistent with Cl- uptake by a Na+-Cl- or Na+-K+-2Cl- cotransport mechanism rather than Cl(-)-HCO3(-)-OH- exchange coupled to Na+-H+ exchange. Incubation in low [Na+] or [Cl-] before stimulation with forskolin (0.1 mM) reduced both peak and sustained Isc, and saturation kinetics were exhibited. Hill coefficients for [Na+] and [Cl-] were 0.99 and 1.04, respectively, for peak Isc and 0.66 and 1.18, respectively, for sustained Isc. Apparent ion affinities for Na+ and Cl- were 13.5 and 18 mM, respectively, for peak Isc and 15 and 22 mM, respectively, for sustained Isc. These results favor Cl- uptake by a 1 Na+:1 Cl- cotransport mechanism for the rabbit corneal epithelium, but involvement of K+ in this process has not been eliminated.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1990

Mechanisms underlying volume regulatory decrease by Necturus gallbladder epithelium.

Volume regulatory decrease (VRD) by Necturus gallbladder epithelial cells in Cl Ringer was unaffected by the addition of 5 mM BaCl2 to apical perfusates but was inhibited by the addition of 5 mM BaCl2 and 50 or 3 microM phencyclidine (PCP) to serosal perfusates, suggesting that K channels in the basolateral membrane were activated during VRD. VRD was unaffected by replacement of Cl with NO3 or SCN, suggesting that Cl-dependent Na-K-Cl and K-Cl cotransport were not involved. In SCN Ringer, VRD was inhibited by the addition of 0.1 mM bumetanide to serosal perfusates, suggesting that bumetanide-sensitive anion channels in the basolateral membrane were also activated. A transient 10-mV hyperpolarization of the membrane potential was associated with VRD. The channel blockers that inhibited VRD had little or no effect on the hyperpolarization, suggesting that the changes in membrane potential were unrelated to the changes in cell volume. Perfusion of the apical surface of the epithelium with isotonic solutions containing 10 mM D-glucose resulted in a variable increase in cell volume followed by a variable shrinkage to normal, suggesting that VRD was also activated during organic solute absorption. The increase in cell volume was blocked by the addition of 0.01 or 1 mM phlorizin to mucosal perfusates. The reduction in cell volume was inhibited by the addition of 0.1 mM bumetanide, but not BaCl2 or PCP, to serosal perfusates, indicating the the shrinkage mechanism secondary to glucose addition differed from that seen after exposure to hypotonic perfusates.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1993

Effect of osmotic swelling and shrinkage on Na(+)-K+ pump activity in mammalian cardiac myocytes.

The effect on the sarcolemmal Na(+)-K+ pump of exposure to anisosmolar solutions was examined using whole cell patch clamping and ion-selective microelectrodes. Na(+)-K+ pump currents were measured in single ventricular myocytes by using pipette Na+ concentrations ([Na]pip) of 0-70 mM. The relationship between [Na]pip and pump current was well described by the Hill equation. The [Na]pip for half-maximal pump current (K0.5) was 21.4 mM in isosmolar (310 mosM) solution. K0.5 was 12.8 mM during cell swelling in hyposmolar solution (240 mosM) and 39.0 mM during cell shrinkage in hyperosmolar solution (464 mosM). The maximal pump currents, derived from the best fit of the Hill equation, and the Hill coefficients were similar in isosmolar, hyposmolar, and hyperosmolar solutions. A sustained (> 20 min) decrease in the intracellular Na+ activity developed during exposure of intact papillary muscles to hyposmolar solutions, and a sustained increase developed during exposure to hyperosmolar solutions. We conclude that osmotic myocyte swelling stimulates the sarcolemmal Na(+)-K+ pump at near-physiological levels of intracellular Na+, whereas shrinkage inhibits the pump. These changes are due to increases and decreases, respectively, in the apparent affinity of the pump for Na+.

Animals↗
PubMed1993

Control of intracellular calcium by membrane potential in human melanoma cells.

The modulation of intracellular calcium ([Ca2+]i) by the membrane potential was investigated in human melanoma cells by combining the nystatin-perforated patch-clamp technique with Ca2+ measurements. Voltage steps to -100 mV induced a rise in [Ca2+]i and a creeping inward current. These effects were absent in Ca(2+)-free solution and could be blocked by Ni2+ or La3+. Voltage ramps revealed a close correlation between [Ca2+]i and voltage, with the strongest voltage dependence around the resting potential. Long-lasting tail currents, closely correlated with the rise in [Ca2+]i and a reversal potential close to the K+ equilibrium potential, occurred if the membrane potential was clamped back to 0 mV. They were absent if intracellular K+ was replaced by Cs+ and blocked by extracellular tetraethylammonium (5 mM), Ba2+ (1 mM), or a membrane-permeable adenosine 3',5'-cyclic monophosphate analogue. These observations are discussed in relation to cell proliferation. The enhanced expression of K+ channels during cell proliferation provides a positive-feedback mechanism resulting in long-term changes in [Ca2+]i required for the G1-S transition in the cell cycle.

Barium↗
PubMed1994

Volume regulation in cultured cells derived from human retinal pigment epithelium.

To characterize volume regulatory mechanisms, unidirectional Rb+ efflux and influx, unidirectional Cl- influx, and cell volume were measured in cultured human retinal pigment epithelium (HRPE). The HRPE was found to be capable of both regulatory volume increase (RVI), in response to a hypertonic challenge, and regulatory volume decrease (RVD), in response to a hypotonic challenge. Bumetanide-sensitive Rb+ influx increased almost threefold on incubation in a hypertonic (390 mosmol/kgH2O) medium. Bumetanide-insensitive Rb+ influx was activated by hypotonic (190 mosmol/kgH2O) challenge as well as by treatment with N-ethylmaleimide (NEM). Exposure to hypotonic media also activated unidirectional Cl- influx and unidirectional Rb+ efflux. Both the RVD and hypotonically activated Rb+ efflux were inhibited by the K(+)-channel blocker barium. On the other hand, hypotonically activated Rb+ influx was increased by barium treatment. In sum, the HRPE exhibits volume-sensitive transport mechanisms over a range of volumes from 190 to 390 mosmol/kgH2O. Cultured HRPE possess hypertonically activated Na-K-Cl cotransport, hypotonically activated K-Cl cotransport, and a barium-inhibitable hypotonically activated K+ efflux pathway.

Barium Compounds↗
PubMed1997

Growth factor-mediated K+ channel activity associated with human myeloblastic ML-1 cell proliferation.

ML-1 cell proliferation is dependent on the presence of serum growth factors. Removing serum from the culture medium results in growth arrest and promotes differentiation. In this study, we found that a 4-aminopyridine-sensitive K+ channel was highly expressed in proliferating ML-1 cells and significantly diminished in G1-arrested ML-1 cells induced by serum deprivation but was restored within 30 min in these cells with addition of 10% fetal bovine serum (FBS) or 5 ng/ml epidermal growth factor (EGF). Intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels, but not guanosine 3',5'-cyclic monophosphate, were significantly increased in serum-deprived cells stimulated by FBS or EGF, and the effects of FBS and EGF on the channel activation were mimicked by exogenous cAMP. In inside-out patches, K+ channel activity was significantly increased by the cAMP-dependent protein kinase catalytic subunit, whereas the effect of EGF on K+ channel activation was blocked by Rp-8-(4-chlorophenylthio)adenosine 3',5'-cyclic monophosphothioate. Together, our results demonstrate that serum growth factors stimulate K+ channel activity in proliferation of ML-1 cells through protein kinase-induced phosphorylation and suggest an important molecular mechanism for serum growth factor-stimulated mitogenesis in ML-1 cells.

4-Aminopyridine↗
PubMed1998

Osmotic pressure regulates alpha beta gamma-rENaC expressed in Xenopus oocytes.

The hypothesis that amiloride-sensitive Na+ channels (ENaC) are involved in cell volume regulation was tested. Anisosmotic ND-20 media (ranging from 70 to 450 mosM) were used to superfuse Xenopus oocytes expressing alpha beta gamma-rat ENaC (alpha beta gamma-rENaC). Whole cell currents were reversibly dependent on external osmolarity. Under conditions of swelling (70 mosM) or shrinkage (450 mosM), current amplitude decreased and increased, respectively. In contrast, there was no change in current amplitude of H2O-injected oocytes to the above osmotic insults. Currents recorded from alpha beta gamma-rENaC-injected oocytes were not sensitive to external Cl- concentration or to the K+ channel inhibitor BaCl2. They were sensitive to amiloride. The concentration of amiloride necessary to inhibit one-half of the maximal rENaC current expressed in oocytes (Ki; apparent dissociation constant) decreased in swollen cells and increased in shrunken oocytes. The osmotic pressure-induced Na+ currents showed properties similar to those of stretch-activated channels, including inhibition by Gd3+ and La3+, and decreased selectivity for Na+. alpha beta gamma-rENaC-expressing oocytes maintained a nearly constant cell volume in hypertonic ND-20. The present study is the first demonstration that alpha beta gamma-rENaC heterologously expressed in Xenopus oocytes may contribute to oocyte volume regulation following shrinkage.

Amiloride↗
PubMed2000

Stimulation of unitary T-type Ca(2+) channel currents by calmodulin-dependent protein kinase II.

The effect of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) stimulation on unitary low voltage-activated (LVA) T-type Ca(2+) channel currents in isolated bovine adrenal glomerulosa (AG) cells was measured using the patch-clamp technique. In cell-attached and inside-out patches, LVA channel activity was identified by voltage-dependent inactivation and a single-channel conductance of approximately 9 pS in 110 mM BaCl(2) or CaCl(2). In the cell-attached patch, elevation of bath Ca(2+) from 150 nM to 1 microM raised intracellular Ca(2+) in K(+)-depolarized (140 mM) cells and evoked an increase in the LVA Ca(2+) channel probability of opening (NP(o)) by two- to sixfold. This augmentation was associated with an increase in the number of nonblank sweeps, a rise in the frequency of channel opening in nonblank sweeps, and a 30% reduction in first latency. No apparent changes in the single-channel open-time distribution, burst lengths, or openings/burst were apparent. Preincubation of AG cells with lipophilic or peptide inhibitors of CaMKII in the cell-attached or excised (inside-out) configurations prevented the rise in NP(o) elicited by elevated Ca(2+) concentration. Furthermore, administration of a mutant recombinant CaMKIIalpha exhibiting cofactor-independent activity in the absence of elevated Ca(2+) produced a threefold elevation in LVA channel NP(o). These data indicate that CaMKII activity is both necessary and sufficient for LVA channel activation by Ca(2+).

Animals↗
PubMed2001

Endothelin-1 decreases glutamate uptake in primary cultured rat astrocytes.

Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that is also known to induce a wide spectrum of biological responses in nonvascular tissue. In this study, we found that ET-1 (100 nM) inhibited the glutamate uptake in cultured astrocytes expressing the glutamate/aspartate transporter (GLAST); astrocytes did not express the glutamate transporter-1 (GLT-1). The V(max) and the K(m) of the glutamate uptake were reduced by 57% and 47%, respectively. Application of the ET(A) and ET(B) receptor antagonists BQ-123 and BQ-788 partly inhibited the ET-1-evoked decrease in the glutamate uptake, whereas the nonspecific ET receptor antagonist bosentan completely inhibited this decrease. Incubation of the cultures with pertussis toxin abolished the effect of ET-1 on the uptake. The ET-1-induced decrease in the glutamate uptake was independent of extracellular free Ca(2+) concentration, whereas the intracellular Ca(2+) antagonists thapsigargin and 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester abolished the effect of ET-1 on the glutamate uptake. Incubation with the protein kinase C (PKC) antagonist staurosporine, but not with the fatty acid-binding protein bovine serum albumin, prevented the ET-1-induced decrease in the glutamate uptake. These results suggest that ET-1 impairs the high-affinity glutamate uptake in cultured astrocytes through a G protein-coupled mechanism, involving PKC and changes in intracellular Ca(2+).

Amino Acid Sequence↗
PubMed2000

Bone as an ion exchange system: evidence for a pump-leak mechanism devoted to the maintenance of high bone K(+).

To provide evidence of active accumulation of K(+) in bone extracellular fluid (BECF), electric currents driven by damaged living metatarsal bones of weanling mice, immersed in physiological media at different [K(+)], in the presence of blockers of the K(+) channels or of the Na(+)-K(+-)ATPase inhibitor, were measured by means of a voltage-sensitive two-dimensional vibrating probe. At 4 mM extracellular K(+) concentration ([K(+)](o)), an inward steady current density (7.85-38.53 microA/cm(2)) was recorded at the damage site, which was significantly dependent on [K(+)](o). At [K(+)](o) equal to that of BECF (25 mM), current density was reduced by 76%. At [K(+)](o) of 0 mM, the current density showed an increase, which was hindered by tetraethylammonium (TEA). Basal current density was reduced significantly after exposure to TEA or BaCl(2) and was unchanged after long- term exposure to ouabain. By changing control medium with a chloride-free medium, current density was reversed. The results support the view that K(+) excess in bone is maintained by a biologically active cellular system. Because the osteocyte-bone lining cell syncytium was at the origin of the current in bone, it is likely that this system controls the ionic composition of BECF.

Animals↗
PubMed2002

Characterization of regulatory volume decrease in freshly isolated mouse cholangiocytes.

Cell volume regulation plays a vital role in many cell functions. Recent study indicates that both K(+) and Cl(-) channels are important for the regulatory volume decrease (RVD) of cholangiocarcinoma cells, but its physiological significance is unclear due to the tumorous nature of the cells used. This present study reports the RVD of normal mouse cholangiocytes by using freshly isolated bile duct cell clusters (BDCC). A relatively simple and practical method of measuring the cross-sectional area of BDCCs by quantitative videomicroscopy was used to indirectly measure their volumes. Mouse cholangiocytes exhibited RVD, which was inhibited by 5-nitro-2'-(3-phenylpropylamino)-benzoate, DIDS, and glibenclamide, suggesting its dependence on certain chloride channels, such as volume-activated chloride channels. It is also inhibited by barium chloride but not by tetraethylammonium chloride, indicating its dependence on certain potassium channels. However, cAMP agonists had no significant effect on the RVD of BDCCs. This indirect method described can be used to study the RVD of cholangiocytes from normal as well as genetically altered mouse livers.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1989

Effect of hypertonic stress on liver cell volume, bile flow, and volume-regulatory K+ fluxes.

Net hepatic uptake and release of K+ were studied in the isolated-perfused rat liver subjected to a 10-min period of hyperosmotic stress by addition of 80 mM mannitol or sucrose to the perfusing solution. Bile flow and effluent Na+, K+, and Ca2+ activities were monitored throughout. Upon initiation of hypertonic stress, a sharp transient dilution of effluent ion activities indicated hepatic water losses that were larger and occurred more rapidly with sucrose than with mannitol. During continuous hyperosmotic perfusion, portocaval differences in K+ uncovered a steady net influx of the ion into the liver that reached a higher maximum and led to a greater accumulation in experiments with sucrose compared with mannitol. This hepatic K+ uptake was completely blocked by 1 mM ouabain. Upon return to isotonic conditions, a sharp transient concentration of effluent ion activities suggested hepatic water uptake that was again more rapid and pronounced in sucrose- than mannitol-treated livers. This was followed by a transient phase of net hepatic K+ release whose magnitude and duration were proportional to the water movements induced by the removal of each carbohydrate. Administration of 2 mM Ba2+ abolished this K+ efflux. These results indicate that mannitol equilibrates between extra- and intracellular compartments, whereas sucrose apparently does not. The data also suggest that net movements of K+ may be involved in the regulatory volume responses induced by hyperosmotic stress and return to normal tonicity, respectively.

Animals↗
PubMed1998

Secretory effects of ATP on nontransformed dog pancreatic duct epithelial cells.

Extracellular triphosphate nucleotides, such as ATP, may regulate various cellular functions through specific cell surface receptors. We examine in this report the different secretory effects of ATP and analogs on nontransformed dog pancreatic duct epithelial cells (PDEC). We observed that 1) ATP, UTP, adenosine 5'-O-(3-thiotriphosphate), and, to a lesser extent, beta, gamma-methylene-ATP, but not adenosine, stimulated 125I- efflux from PDEC, suggesting a primary role for P2Y2 receptors, 2) ATP-stimulated 125I- efflux was inhibited by 5-nitro-2-(3-phenylpropylamino)benzoic acid, diphenylamine-2-carboxylate, and DIDS, suggesting mediation through Ca2+-activated Cl- channels, 3) ATP stimulated an 86Rb+ efflux sensitive to BaCl2 and charybdotoxin, thus likely occurring through Ca2+-activated K+ channels, 4) serosal or luminal addition of UTP activated apical Cl- conductance and basolateral K+ conductance when nystatin-permeabilized PDEC were studied in an Ussing chamber, suggesting the expression of P2Y2 receptors on both sides of the cell, 5) ATP stimulated mucin secretion, and 6) ATP increases intracellular Ca2+ concentration ([Ca2+]i). In conclusion, ATP and UTP interact with P2Y2 receptors on nontransformed PDEC to increase [Ca2+]i, stimulate mucin secretion, and activate ion conductances; these findings have implications for pancreatic exocrine function in both health and disease, such as cystic fibrosis.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed2000

Luminal ammonia retards restitution of guinea pig injured gastric mucosa in vitro.

The present study was conducted to elucidate the mechanisms by which Helicobacter pylori (HP)-derived ammonia causes gastric mucosal injury. Intact sheets of guinea pig gastric fundic mucosae were incubated in Ussing chambers. Both the luminal and the serosal pH were kept at 7.4. Transmucosal potential difference (PD) and electrical resistance (R) were monitored as indices of mucosal integrity. Restitution was evaluated by recovery of PD, R, and transmucosal [(3)H]mannitol flux after Triton X-100-induced mucosal injury. The effects of luminal or serosal NH(4)Cl on function and morphology of uninjured or injured mucosae were examined. In uninjured mucosae, serosal NH(4)Cl induced more profound decreases in PD and R and more prominent vacuolation in gastric epithelial cells than did luminal NH(4)Cl. In contrast, luminal NH(4)Cl markedly inhibited restitution in injured mucosae and caused an extensive vacuolation in gastric epithelial cells, as did serosal NH(4)Cl. Transmucosal ammonia flux was greater in the injured than in the uninjured mucosae. These results suggest that 1) basolateral membrane of gastric epithelial cells is more permeable to ammonia than apical membrane and 2) luminal ammonia, at concentrations detected in HP-infected gastric lumen, retards restitution in injured mucosae.

Ammonia↗
PubMed2005

Regional ventricular wall thickening reflects changes in cardiac fiber and sheet structure during contraction: quantification with diffusion tensor MRI.

Dynamic changes of myocardial fiber and sheet structure are key determinants of regional ventricular function. However, quantitative characterization of the contraction-related changes in fiber and sheet structure has not been reported. The objective of this study was to quantify cardiac fiber and sheet structure at selected phases of the cardiac cycle. Diffusion tensor MRI was performed on isolated, perfused Sprague-Dawley rat hearts arrested or fixed in three states as follows: 1) potassium arrested (PA), which represents end diastole; 2) barium-induced contracture with volume (BV+), which represents isovolumic contraction or early systole; and 3) barium-induced contracture without volume (BV-), which represents end systole. Myocardial fiber orientations at the base, midventricle, and apex were determined from the primary eigenvectors of the diffusion tensor. Sheet structure was determined from the secondary and tertiary eigenvectors at the same locations. We observed that the transmural distribution of the myofiber helix angle remained unchanged as contraction proceeded from PA to BV+, but endocardial and epicardial fibers became more longitudinally orientated in the BV- group. Although sheet structure exhibited significant regional variations, changes in sheet structure during myocardial contraction were relatively uniform across regions. The magnitude of the sheet angle, which is an index of local sheet slope, decreased by 23 and 44% in BV+ and BV- groups, respectively, which suggests more radial orientation of the sheet. In summary, we have shown for the first time that geometric changes in both sheet and fiber orientation provide a substantial mechanism for radial wall thickening independent of active components due to myofiber shortening. Our results provide direct evidence that sheet reorientation is a primary determinant of myocardial wall thickening.

Animals↗
PubMed1988

Delayed rectifier K+ current in embryonic chick heart ventricle.

Single ventricular cells from 7- to 10-day-old embryonic chicks were studied with the use of whole cell, outside-out, and cell-attached patch-clamp techniques. The macroscopic delayed rectifier current, IK, activated at membrane potentials above -25 mV. Peak IK at +40 mV was 103 +/- 20 pA (5.7 +/- 1 microA/cm2). IK was selective for K ions with reversal potentials close to the Nernst equilibrium potentials. The onset of current during a voltage step was sigmoidal and was fit by the function IK = IKoo (1-e-t/tau)2. The peak time constant of activation was greater than 6 s at -25 mV (22 degrees C). Significant inactivation was not observed. IK was blocked by intracellular cesium, extracellular 1 mM 4-aminopyridine, 20 mM tetraethylammonium chloride, and 1 mM barium chloride. Single-channel recordings revealed a K+-selective channel with a slope conductance of 15 pS (extracellular [K+] = 4 mM, intracellular [K+] = 145 mM). An ensemble average of consecutive single-channel traces reproduced the whole cell current. The single-channel density was approximately 0.04/micron 2 based on frequency of patches containing the 15-pS single conductance. Approximately 100 channels/cell would sum to account for the net IK. We have described for the first time a channel underlying the main delayed rectifier current and, as such, a main repolarization current in chick ventricle.

4-Aminopyridine↗