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PubMed1994

Fluctuations in Fe, Cu, Zn, Br, As, Se, and Rb concentrations in C57L/J mice bearing BW7756 murine hepatoma using radioisotope-induced X-ray fluorescence.

The effects of selenite or selenate supplementation on the concentration and distribution of Fe, Cu, Zn, As, Br, and Rb are investigated using the radioisotope-induced X-ray fluorescence, RIXRF. These effects are studied in the animals bearing BW7756 murine hepatoma and healthy animals for both of the oxidation states. Selenite and selenate induce different effects on the distribution of selenium, zinc, copper, bromine, and rubidium. The differences may be attributed to the differences in the inter element interaction after absorption into the bloodstream as well as to the mode of their intestinal absorption. Simultaneous supplementation of copper with selenite or selenate at the described levels has a profound influence on the concentration levels of other elements in the normal as well as in the diseased mice. The administration of selenium (0.67 micrograms/g body wt sodium selenite or sodium selenate, daily) and selenium and copper (0.67 and 1.35 micrograms/g body wt, respectively) has no effect on the incidence rate of hepatoma development.

Animals↗
PubMed2000

Potassium and sodium fluxes in the phytopathogenic fungus Fusarium oxysporum var. lini.

Rubidium uptake in potassium-starved cells followed biphasic kinetics in the micromolar and millimolar range and was independent of the temperature. In contrast, Rb(+) uptake in normal-K(+) cells followed a monophasic kinetics in the millimolar range and increased at temperatures higher than 30 degrees C. Differences in the K(m) values and in the Arrhenius plots of Rb(+) uptake suggest different uptake systems in K(+)-starved and in normal-K(+) cells. In addition, the substantial inhibition of Rb(+) uptake caused by carbonyl cyanide-m-chlorophenyl hydrazone indicates that these systems are strongly dependent on membrane voltage. Lithium (sodium) tolerance, influx, and efflux were separately studied. F. oxysporum was shown to be very tolerant to sodium, while lithium caused a specific toxic effect. Li(+) uptake in K(+)-starved cells exhibits a monophasic kinetics with low affinity. Li(+) efflux was not affected by external pH or addition of potassium to the medium, suggesting that a Na(+)/cation antiporter is not involved in this process.

Carbonyl Cyanide m-Chlorophenyl Hydrazone↗
PubMed2000

Muscarinic down-regulation of cAMP-stimulated potassium ion secretion by rabbit distal colon.

The sustained effects of the cholinergic agonist carbachol (CCh) on electrolyte transport across the isolated, short-circuited rabbit distal colon were examined in the absence and presence of secretagogue (di-butyryl cyclic-adenosine monophosphate, dB-cAMP). Steady-state, basal absorption of 22Na+, 42K+ (86Rb+), and 36Cl- were not significantly altered by addition of the CCh (10(-4) mmol/l) to the serosal reservoir. Stimulation with dB-cAMP (1.0 mmol/l, serosal) promoted K+ (or Rb+) and Cl- secretion across the colon, without significantly affecting the unidirectional or net fluxes of Na+. Serosal (but not mucosal) addition of CCh to dB-cAMP-stimulated tissues reduced the serosal to mucosal flux of Rb+ (J(Rb)SM) in a concentration-dependent manner with a half-maximum concentration approximately equal 5 micromol/l. Pretreatment with CCh (100 micromol/l, serosal) inhibited dB-cAMP-induced K+ secretion, but had no significant effect on the steady-state unidirectional fluxes of Na+ or Cl-. Serosal histamine (20 micromol/l) also inhibited J(Rb)SM in dB-cAMP-stimulated tissues. Serosal epinephrine (10 micromol/l) promoted a decrease in short-circuit current (Isc) and transepithelial potential (VT) that was mirrored by increases in J(Rb)SM. Both Isc, and VT became more positive and J(Rb)SM was reduced when CCh was added to the epinephrine-stimulated tissues. Serosal muscarine (50 micromol/l) mimicked the CCh-induced inhibition of J(Rb)SM, but serosal nicotine (50 micromol/l) had no effect. In atropine-treated tissues (1 micromol/l, serosal), CCh failed to block dB-cAMP-stimulated increases in J(Rb)SM. The inhibitory action of CCh was observed in tissues that had been pretreated with 50 micromol/l serosal hexamethonium (a ganglionic transmission blocker) or 2 micromol/l serosal tetrodotoxin (a voltage-gated Na+ channel blocker), indicating that the inhibitory action of this cholinergic agonist does not depend on remnant enteric neural pathways. Rubidium ion transport across confluent monolayers of T84 cells was similarly affected by dB-cAMP and CCh, supporting the notion that enteric neural pathways are not required. Serosal charybdotoxin (20 nmol/l) mitigated the inhibitory action of CCh on J(Rb)SM in dB-cAMP-stimulated tissues, suggesting a role for basolateral, Ca2+-dependent K+ channels in the actions of CCh. It is concluded that basolateral muscarinic receptors (and possibly other Ca2+-dependent receptor pathways) of secretory colonocytes mediate the down-regulation of potassium ion secretion by rabbit distal colon, possibly by increasing basolateral membrane K+ conductance.

Animals↗
PubMed1997

Changes in subsarcolemmal sodium concentration measured by Na-Ca exchanger activity during Na-pump inhibition and beta-adrenergic stimulation in guinea-pig ventricular myocytes.

Measurement of Na-Ca exchange activity was used to examine subsarcolemmal sodium levels ([Na+]s) in single, voltage-clamped guinea-pig cardiac myocytes while Na-K pump activity was modulated pharmacologically. Changes in Nas were evaluated from phase-plane analysis of the changes in intracellular calcium, measured using the fluorescent indicators Fura-red and Fluo-3. Activation of beta-adrenoceptors with 1 microM isoprenaline resulted in activation of the cAMP-dependent chloride current, but had no effect on the calcium transient mediated via the Na-Ca exchanger, regardless of whether the Na-K pump was active or inhibited (with strophanthidin). The ability of Na-Ca exchange activity to report [Na+]s was demonstrated by the effect of changing the extracellular rubidium concentration from 1 to 5.4 mM to modulate Na-K pump activity. We suggest that beta-adrenergic stimulation does not directly affect either the Na-K pump or the Na-Ca exchanger and that the Na-Ca exchanger can be used as a sensitive indicator of changes in [Na+]s and Na-K pump activity.

Adrenergic beta-Agonists↗
PubMed2006

Protein kinase C family members as a target for regulation of blood-brain barrier Na,K,2Cl-cotransporter during in vitro stroke conditions and nicotine exposure.

PURPOSE: The aim of the study is to identify specific protein kinase C (PKC) isoforms involvement in K(+) transport mediated at altered blood-brain barrier (BBB) response to stroke conditions with prior nicotine exposure, which provides ways to intervene pharmacologically in PKC-mediated molecular pathways that could lead to effective treatment for smoking stroke patients. METHODS: Changes in PKC isoform levels were studied in the cytosolic and membrane fractions of bovine brain microvessel endothelial cells subjected to stroke conditions as well as nicotine/cotinine exposure. Furthermore, abluminal Na,K,2Cl-cotransporter (NKCC) activity regulated by specific conventional PKC isoform activators and inhibitors was investigated using rubidium ((86)Rb) uptake studies. RESULTS: Membrane-bound PKCalpha, PKCbetaI, and PKCepsilon levels were increased after 6 h hypoxia/aglycemia, and this was attenuated by 24-h nicotine/cotinine exposure. Interestingly, membrane-bound PKCgamma protein level was decreased after 6 h hypoxia/aglycemia and increased by 24-h nicotine/cotinine exposure. (86)Rb uptake studies showed that basolateral NKCC activity was down-regulated by both a conventional PKC inhibitor and specific inhibitors for PKCalpha, PKCbeta, and PKCvarepsilon and was up-regulated by an activator of conventional PKCs during 6-h hypoxia/aglycemia treatment. CONCLUSION: Specific PKC inhibitors or activators might be designed to individualize stroke therapies and improve health outcome for smokers by rebalancing ion transport into and out of the brain.

Animals↗
PubMed1987

Asymptomatic myocardial ischemia following cold provocation.

Cold is thought to provoke angina in patients with coronary disease either by an increase in myocardial demand or an increase in coronary vascular resistance. We investigated and compared the effects of cold pressor stimulation and symptom-limited supine bicycle exercise on regional myocardial perfusion in 35 patients with stable angina and coronary disease and in 10 normal subjects. Regional myocardial perfusion was assessed with positron emission tomography and rubidium-82. Following cold pressor stimulation 24 of 35 patients demonstrated significant abnormalities of regional myocardial perfusion with reduced cation uptake in affected regions of myocardium: 52 +/- 9 to 43 +/- 9 (p less than 0.001 vs normal subjects). Among these 24 patients only nine developed ST depression and only seven had angina. In contrast, 29 of 35 patients underwent supine exercise, and abnormal regional myocardial perfusion occurred in all 29, with a reduction in cation intake from 48 +/- 10 to 43 +/- 14 (p less than 0.001 vs normal subjects). Angina was present in 27 of 29 and ST depression in 25 of 29. Although the absolute decrease in cation uptake was somewhat greater following cold as opposed to exercise, the peak heart rate after cold was significantly lower than that after exercise (82 +/- 12 vs 108 +/- 16 bpm, p less than 0.05). Peak systolic blood pressures after cold and exercise were similar (159 +/- 24 vs 158 +/- 28). Thus, cold produces much more frequent asymptomatic disturbances of regional myocardial perfusion in patients with stable angina and coronary disease than is suggested by pain or ECG changes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Effect of quinidine on differing sensitivities of Purkinje fibers and myocardium to inhibition of monovalent cation transport by digitalis in dogs.

Studies have implicated quinidine in increasing serum digoxin levels, resulting in serious arrhythmias. Arrhythmias caused by digitalis intoxication are thought to originate in Purkinje fibers. Thus, the extent of inhibition of monovalent cation-active transport in Purkinje fibers and myocardium may explain the enhanced toxicity of the combined administration of digoxin and quinidine. Monovalent cation transport was assessed by measuring the uptake of the potassium analog rubidium in samples of myocardium and Purkinje fibers after in vitro exposure to ouabain and after long-term administration of digoxin and quinidine or digoxin alone. A group of dogs received chronic digoxin administration and achieved a steady-stage digoxin administration and achieved a steady-stage digoxin level of 2.1 +/- 0.3 ng/ml. Quinidine administered intravenously caused a 134% increase in the serum digoxin level. The transport in myocardium was unchanged, while it was reduced to 40% of control levels in Purkinje fibers. The difference in sensitivity between Purkinje fibers and myocardium may explain the finding that digitalis-toxic arrhythmias arise in Purkinje fibers and that quinidine, when combined with digitalis, increases the incidence of such arrhythmias.

Animals↗
PubMed1986

Direct effects of smoking on the heart: silent ischemic disturbances of coronary flow.

Cigarette smoking is strongly associated with ischemic heart disease and acute coronary events. The effect of smoking a single cigarette on regional myocardial perfusion was studied in 13 chronic smokers with typical stable angina pectoris using positron emission tomography and rubidium-82 (82Rb). Findings were compared with the effects of physical exercise. After exercise, 8 patients (61%) had angina, ST depression and abnormal regional myocardial perfusion. Uptake of 82Rb increased from 49 +/- 8 to 60 +/- 7 in remote myocardium, but decreased from 46 +/- 3 to 37 +/- 5 in an ischemic area. The remaining 5 patients (39%) had homogeneous increases in 82Rb uptake without angina or ST depression. After smoking, 6 of the 8 patients with positive exercise test responses had a decrease in 82Rb uptake, from 47 +/- 3 to 35 +/- 6 in the same segment of myocardium affected during exercise. However, in contrast to exercise, the events during smoking were largely silent. The absolute decreases in regional 82Rb uptake after smoking occurred at significantly lower levels of myocardial oxygen demand than after exercise. This suggests that an impairment of coronary blood supply is responsible. Thus, in smokers with coronary artery disease, each cigarette can cause profound silent disturbances of regional myocardial perfusion that are likely to occur frequently during daily life. Such repeated insults may represent an important mechanism linking smoking with coronary events.

Adult↗
PubMed1987

Beneficial effect of nitrates on myocardial glucose utilization in unstable angina pectoris.

Myocardial uptake of the glucose analog F-18-2-fluoro-2-deoxy-D-glucose (FDG) was assessed by positron emission tomography in 6 normal volunteers, 7 patients with chronic stable angina and 22 patients with unstable angina at rest in fasting conditions. Regional myocardial perfusion was assessed by rubidium-82. The study was repeated a few days later after intravenous infusion of isosorbide dinitrate. FDG uptake was similar in control subjects and patients with stable angina (0.023 +/- 0.032 vs 0.012 +/- 0.008 mol/ml/min, p less than 0.42) but was about 4-fold higher on the average in patients with unstable angina (0.084 +/- 0.047, p less than 0.01). The severity of coronary obstructions in stable and unstable angina patients was similar. The increased uptake involved the whole heart, including areas not distal to critically stenosed vessels; it was not associated with reduced myocardial perfusion and was not related to a recent episode of transient ischemia as assessed by symptoms and by Holter monitoring. After continuous infusion of nitrates, FDG uptake was consistently and significantly reduced toward normal levels both in areas perfused by critically stenosed coronary arteries and by noncritically stenosed vessels.

Adult↗
PubMed1978

Chemically-induced cation permeability in red cell membrane vesicles. The sidedness of the response and the proteins involved.

Cation fluxes were measured in right-side-out and inside-out vesicles obtained from human red cells. Rubidium, which is spontaneously released at very slow rates, can be rapidly released from both types of vesicle by addition of valinomycin. P-Chloromercuriphenyl sulfonic acid (PCMBS) also increases the cation permeability of the vesicles with reversal to normal after addition of dithiothreitol. The effect of PCMBS is considerably larger and appears faster in the inside-out vesicles as compared to the right-side-out vesicles, the difference being greater at low temperatures. These data indicate that the SH groups responsible for the changes in cation permeability are more accessible from the inside face of the membrane. The response to PCMBS was not diminished after selective removal of extrinsic proteins by alkaline extraction, and/or after the membranes were exposed to proteolytic enzymes. The major polypeptide component remaining in vesicles after both treatments was a 17 000-dalton transmembrane fragment derived from band 3 which might, therefore, be responsible for the permeability response. Addition of Ca2+ to either right-side-out or inside-out vesicles, in the presence or absence of ionophore A23187, was without effect on monovalent cation permeability, indicating that the mechanism of Ca2+-induced K+ permeation was lost or inactivated during the preparation of the vesicles.

4-Chloromercuribenzenesulfonate↗
PubMed1988

Bile salt-induced calcium fluxes in artificial phospholipid vesicles.

The ionic permeability of selected biological membranes is increased by bile salts. To examine changes in calcium permeability during the exposure of artificial membranes to bile salts, we investigated calcium uptake by unilamellar and multilamellar phospholipid vesicles. In the presence of 750 microM taurodeoxycholate, uptake of radiolabelled calcium by unilamellar vesicles increased 2.5-fold over control values. Calcium uptake by multilamellar vesicles as measured with a free calcium indicator, arsenazo III, increased 2.2- or 21-fold in the presence of 60 microM lithocholate or 3 beta-hydroxy-5-cholenoate, respectively. Results were directly influenced by experimental variables such as bile salt hydrophobicity, external calcium concentration, and the bile salt/lipid molar ratio. Observed membrane solubilization was minimal despite increased calcium permeability. Comparison of radiolabelled calcium uptake with radiolabelled sodium or radiolabelled rubidium uptake indicated that bile salt-dependent calcium uptake was 60-140-times greater than bile salt-dependent uptake of either monovalent cation. In an effort to delineate forces affecting calcium translocation, vesicles were exposed either to valinomycin, which induced an electrochemical gradient across the membrane, or to nigericin, which induced a proton gradient. Exposure to valinomycin minimally influenced bile salt-induced calcium uptake while exposure to nigericin significantly promoted uptake by 40-70%. The results suggest that bile salts promote calcium uptake by a mechanism which may be similar to those of other carboxylic ionophores.

Arsenazo III↗
PubMed1988

Effects of L-alanine on membrane potential, potassium (86Rb) permeability and cell volume in hepatocytes from Raja erinacea.

Isolated hepatocytes from the elasmobranch Raja erinacea were examined for their regulatory responses to a solute load following electrogenic uptake of L-alanine. The transmembrane potential (Vm) was measured with glass microelectrodes filled with 0.5 M KCl (75 to 208 M omega in elasmobranch Ringer's solution) and averaged -61 +/- 16 mV (S.D.; n = 68). L-Alanine decreased (depolarized) Vm by 7 +/- 3 and 18 +/- 2 mV at concentrations of 1 and 10 mM, respectively. Vm did not repolarize to control values during the 5-10 min impalements, unless the amino acid was washed away from the hepatocytes. The depolarizing effect of L-alanine was dependent on external Na+, and was specific for the L-isomer of alanine, as D- and beta-alanine had no effect. Hepatocyte Vm also depolarized on addition of KCN or ouabain, or when external K+ was increased. Rates of 86Rb+ uptake and efflux were measured to assess the effects of L-alanine on Na+/K+-ATPase activity and K+ permeability, respectively. Greater than 80% of the 86Rb+ uptake was inhibited by 2 mM ouabain, or by substitution of choline+ for Na+ in the incubation media. L-Alanine (10 mM) increased 86Rb+ uptake by 18-49%, consistent with an increase in Na+/K+ pump activity, but had no effect on rubidium efflux. L-Alanine, at concentrations up to 20 mM, also had no measurable effect on cell volume as determined by 3H2O and [14C]inulin distribution. These results indicate that Na+-coupled uptake of L-alanine by skate hepatocytes is rheogenic, as previously observed in other cell systems. However, in contrast to mammalian hepatocytes, Vm does not repolarize for at least 10 min after the administration of L-alanine, and changes in cell volume and potassium permeability are also not observed.

Alanine↗
PubMed1990

The effects of a low extracellular concentration of potassium on the activity and numbers of Na+/K+ pumps in an EB-virus transformed human lymphocyte cell line.

The BM1A EB-virus transformed human lymphocyte cell line contains approximately 950,000 Na+/K(+)-ATPase sites per cell. The turnover number of each site is approx. 2240 molecules of rubidium per min. When cells are exposed to a low extracellular concentration of potassium the intracellular concentration of sodium rises, and the cells respond in the short term by increasing the Vmax of 86Rb+ uptake. In the longer term the cells respond by increasing both the Vmax of 86Rb+ uptake and the Bmax of [3H]ouabain binding. The suggestion that increases in the intracellular concentration of sodium is responsible for these changes is supported by the finding that monensin, which increases intracellular sodium without affecting intracellular potassium, is capable of inducing both the short- and long-term changes associated with a low external concentration of potassium.

5'-Nucleotidase↗
PubMed1976

Effects of alkali metal cations on phospho-enzyme levels and [3H] ouabain binding to (Na+ + K+)-ATPase.

The effects of several alkali metal cations on the relationship between steady state phospho-enzyme levels and initial velocity and equilibrium levels of [3H]-ouabain binding to (Na+ + K+)-ATPase (ATP phosphohydrolase EC 3.6.1.3.) were examined. Only Na+ increased both phospho-enzyme and [3H] ouabain binding levels above those observed in the presence of Mg2+ alone. While Na+ stimulated phosphorylation with an apparent Km of about 1 mM, its stimulation of [3H] ouabain binding was biphasic, the lower Km for stimulation corresponding to the Km for formation of phospho-enzyme. Among the other alkali metal cations, potassium, rubidium and lithium were at least eight times more effect in reducing phospho-enzyme levels than in reducing [3H] ouabain binding. This discrepancy is not due to the stability of the enzyme-ouabain complex, nor to any action on the rates of formation or dissociation of the enzyme-ouabain complex. The data thus suggest that [3H] ouabain interacts with the K+, Rb+ or Li+ -enzyme complexes. For Li+, this hypothesis is further supported by the observation that Li+ can cirectly increase the equilibrium level of [3H] ouabain binding to this enzyme under certain conditions.

Adenosine Triphosphatases↗
PubMed1992

Hepatocyte growth factor is a paracrine factor for renal epithelial cells: stimulation of DNA synthesis and NA,K-ATPase activity.

The expressions of mRNAs of hepatocyte growth factor (HGF) and its receptor (c-met) and its effects were examined in cultured renal epithelial cell lines (OK, LLCPK1, and MDCK cells) and rat mesangial cells in primary culture. Northern blot analysis revealed the presence of HGF mRNA in mesangial cells, but not in epithelial cells. c-met mRNA was detected in epithelial cells, but not in mesangial cells. HGF stimulated [3H]-thymidine incorporation (DNA synthesis) dose-dependently in OK and LLCPK1 cells, but not in MDCK and mesangial cells. Ouabaine sensitive rubidium uptake (Na,K-ATPase activity) was stimulated by 63% with HGF (10 ng/ml) treatment for 16hr in MDCK cells. The results suggest that HGF is produced in the kidney, at least in mesangial cells and works on epithelial cells to stimulate the proliferation and/or to modify cell functions in a paracrine manner.

Animals↗
PubMed1986

The acute in vitro effect of ethanol, its metabolites and other toxic alcohols on ion flux in isolated human leucocytes and erythrocytes.

Using isolated healthy human leucocytes and erythrocytes as model cells, we investigated the inhibitory effect of ethanol, its metabolites and of other toxic alcohols on the active fluxes of rubidium (Rb: equivalent to K) and sodium (Na), and on Na,K-ATPase activity. Ethanol (80 mmol X l-1) inhibited total and ouabain-sensitive 86Rb influx and 22Na efflux in leucocytes, this being dose-related for total, ouabain-sensitive and ouabain-insensitive fluxes at higher concentrations. In erythrocytes inhibition occurred at 20 mmol X l-1 for 86Rb influx, dose-related at higher concentrations as for leucocytes. 22Na efflux was inhibited at 80 mmol X l-1 and above. Acetaldehyde (0.1 and 0.2 mmol X l-1), 1,2-propanediol (0.8 mmol X l-1) and 2,3-butanediol (0.4 mmol X l-1) inhibited all fractions of 86Rb influx in erythrocytes, but not in leucocytes. Methanol, 2-propanol and 1,2-ethanediol (16 and 32 mmol X l-1) inhibited 86Rb influx in erythrocytes, but not in leucocytes. The order of potency was 2-propanol greater than 1,2-ethanediol greater than methanol. Na,K-ATPase activity was inhibited in lysed leucocyte and erythrocyte preparations only at very high concentrations of the alcohols--suggesting that inhibition is due to an alteration in membrane structure and not to a direct effect on the enzyme.

1-Propanol↗
PubMed1992

Reversal of the effects of a low extracellular potassium concentration on the number and activity of Na+/K+ pumps in an Epstein-Barr virus-transformed human lymphocyte cell line.

A reduction in the extracellular concentration of potassium to 0.5 mM (low K) in Epstein-Barr (EB) virus-transformed lymphocytes caused changes in the number and activity of Na+/K+ pumps in the cell membrane, with increases in the Bmax and apparent Kd of ouabain binding, and concomitant increases in the Vmax and apparent Km of potassium (rubidium) influx. However, recovery from the effects of low K occurred more quickly than the original up-regulation. Furthermore, there were differences in the time-courses of the separate rates of recovery of the Bmax and Kd of ouabain binding after the cells were returned to normal K, the rate of recovery of the Kd being quicker than that of the Bmax, which was biphasic, with slow and fast rates of recovery. Inhibition of protein synthesis by emetine caused an increase in the rate of recovery of the Bmax of ouabain binding, but no effect on the Kd, suggesting that the slow phase of recovery of the Bmax is attributable to the synthesis and insertion of new protein, while the rapid phase of recovery is independent of protein synthesis and may represent internalization. The results suggested that during up-regulation of pump number in response to low K about 40% of the newly inserted Na+/K+ pumps are normal and the rest are abnormal. The half-time of removal of the abnormal pumps from the cell membrane during recovery from low K stress was 2.8 hr and the half-time of internalization of the normal pumps was 4.3 hr.

Cell Line, Transformed↗
PubMed1993

4-Aminopyridine reduces chorda tympani nerve taste responses to potassium and alkali salts in rat.

To study the potential role of potassium channels in the taste response to potassium salts, we applied 4-aminopyridine (4-AP) to the anterior rat tongue and recorded chorda tympani nerve taste responses to chemical stimuli. 4-aminopyridine is a pharmacological blocker that reduces potassium conductance through potassium channels in nerve and muscle. Summated neural responses to stimuli dissolved in water and in 4-AP were compared. Chemical stimuli included concentration ranges of KCl, KBr, KH2PO4, CsCl, RbCl, NH4Cl, NaCl and sucrose. The blocker reduced chorda tympani responses to KCl and other potassium salts, from 0.025 to 0.25 M. Responses to ammonium, rubidium and cesium salts also were reduced, in order of effectiveness that would be predicted from known ion selectivity properties of potassium channels. Responses to NaCl and sucrose were not reduced. Other channel blockers, including tetraethylammonium chloride (TEA), BaCl2 and quinidine, did not reduce the response to KCl. These are the first detailed reports of effects of potassium channel blockers on the peripheral, neural taste response. The results are consistent with a role for potassium channels in apical taste bud cell membranes in transduction for potassium salts.

4-Aminopyridine↗