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A Molleman

Publications and source records attributed to A Molleman.

16 recordsLinked to original sources
PubMed2002

Modulation of the release of endogenous adenosine by cannabinoids in the myenteric plexus-longitudinal muscle preparation of the guinea-pig ileum.

1. Interactions between the cannabinoid system and the adenosine system were investigated in the myenteric plexus-longitudinal muscle (MPLM) of the guinea-pig ileum. 2. Electrically-evoked contractions of the MPLM were inhibited in a concentration dependent manner by exogenous adenosine and the adenosine receptor agonist 2-chloroadenosine. These inhibitory effects were reversed by the selective A(1) receptor antagonist DPCPX (20 nM). 3. Preincubation of the MPLM with the cannabinoid receptor agonist CP55,940 (1 nM) or the endogenous cannabinoid ligand anandamide caused a significant leftward shift in the concentration-effect curves to adenosine and 2-chloroadenosine. 4. Electrically-evoked contractions of the MPLM were inhibited in a concentration dependent manner by the adenosine uptake inhibitor dipyridamole. This inhibition was reversed by DPCPX (20 nM). 5. Pretreatment with CP55,940 (1 nM) or anandamide (10 microM) significantly reduced the inhibition produced by dipyridamole, an effect which was completely reversed by the selective CB(1) receptor ligand SR141716 (100 nM). 6. Electrically evoked adenosine release, measured in real time by means of adenosine-specific biosensors, was inhibited by CP55,940 (10 nM). This inhibition was blocked when CP55,940 was applied in the presence of SR141716 (100 nM). 7. These results confirm the presence of presynaptic CB(1) and A(1) receptors in the guinea-pig MPLM, and suggest that CB(1) receptor stimulation reduces electrically-evoked adenosine release. Overall the data raise the possibility that the cannabinoid system plays a role in the modulation of adenosine transmission in the MPLM.

Adenosine↗
PubMed2001

Signal transduction of cannabinoid CB1 receptors in a smooth muscle cell line.

1. The effects of cannabinoid (CB) receptor stimulation on membrane currents in single cells from the Syrian hamster vas deferens cell line DDT1MF-2 were investigated using the whole cell patch clamp technique. 2. The CB receptor agonist CP55,940 evoked a concentration-dependent transient outward current. The selective CB1 receptor ligand SR141716 (1 microM), but not the selective CB2 receptor ligand SR144528 (1 microM), inhibited the outward current. Pertussis toxin (100 ng ml-1 for 20 h) completely abolished the outward current. 3. Western blotting with an antibody against the rat (r)CB1 receptor showed a band characteristic for the CB1 receptor around 63 kDa in DDT1MF-2 cells. 4. The reversal potential for the outward current measured using a voltage ramp protocol was -84 +/- 5 mV. The current was inhibited by the Ca2+-dependent K+ channel blockers iberiotoxin (10 nM) and charybdotoxin (10 nM). 5. Removal of Ca2+ from the bathing solution, or the addition of 0.1 mM Cd2+ completely abolished the outward current evoked by 10 microM CP55,940. 6. The sarcoplasmic Ca2+ pump inhibitor thapsigargin reduced the outward current evoked by 10 microM CP55,940 in a concentration-dependent manner. 7. The mitogen-activating protein kinase (MAP kinase) inhibitor PD98059, but not the phospholipase C inhibitor U73122, inhibited the outward current evoked by 10 microM CP55,940. 8. The adenylyl cyclase inhibitor SQ22,536 (100 microM) and 8-Br-cyclic AMP (10 microM) significantly reduced the outward current evoked by 10 microM CP55,940. 9. Our data suggest that CB1 receptor stimulation in DDT1MF-2 cells leads to activation of a large conductance Ca2+-dependent K+ channel through a Gi/Go protein-mediated rise in [Ca2+]i, for which both inhibition of adenylyl cyclase and activation of MAP kinase are required. In addition, the cannabinoid-induced increase in [Ca2+]i is likely to arise from capacitive Ca2+ entry.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2001

Muscarinic activation of transient inward current and contraction in canine colon circular smooth muscle cells.

Muscarinic receptor mediated membrane currents and contractions were studied in isolated canine colon circular smooth muscle cells. Carbachol (10(-5) M) evoked a slow transient inward current that was superimposed by a transient outward current at holding potentials greater than -50 mV. Carbachol contracted the cells by 70 +/- 2%. The effects of carbachol were blocked by atropine (10(-6) M), tetraethyl ammonium (20 mM), and BAPTA-AM (25 mM applied for 20 min). The inward current and contraction were not sensitive to diltiazem (10(-5) M), nitrendipine (3 x 10(-7) M), niflumic acid (10(-5) M), or N-phenylanthranilic acid (10(-4) M), but were gradually inhibited after repetitive stimulations in Ca2+ free solution. Ni2+ (2 mM) inhibited the inward current by 67 +/- 4%. The inward current reversed at +15 mV. The outward component could be selectively inhibited by iberiotoxin (20 nM) or by intracellular Cs+. Repeated stimulation in the presence of cyclopiazonic acid (CPA, 3 microM) inhibited the carbachol-induced outward current and partially inhibited contraction. CPA did not inhibit the inward current. In conclusion, muscarinic receptor stimulation evoked a CPA-sensitive calcium release that caused contraction and a CPA-insensitive transient inward current was activated that is primarily carried by Ca2+ ions and is sensitive to Ni2+.

Animals↗
PubMed1998

Chronic ethanol administration alters activity in ventral tegmental area neurons after cessation of withdrawal hyperexcitability.

The present study investigated the activity of neurons in the mesolimbic dopamine system after the end of the acute phase of the behavioural signs of ethanol withdrawal in mice. This was designed to provide a comparison with earlier behavioural studies, in which greater development of sensitisation to amphetamine and cocaine, but no change in the initial effects of these compounds, or in the behaviour in the absence of drug treatment, was seen when repeated injection of these psychostimulants were given after chronic ethanol consumption. In the present study, single unit recordings were made from dopamine-sensitive neurons in the ventral tegmental area in perfused midbrain slices prepared 24 h after cessation of chronic ethanol consumption. Profound decreases in firing of the ventral tegmental area (VTA) neurons were seen in slices prepared after the ethanol treatment. Firing rates increased after application of N-methyl-dl-aspartate, but still remained lower and more variable after the ethanol treatment. Application of dopamine or amphetamine, following stimulation of firing with a low concentration of N-methyl-dl-aspartate, also resulted in lower firing rates in slices from ethanol-treated mice. No changes were seen in release of tritiated dopamine, in response to applied KCl or amphetamine, from slices of striatum or cerebral cortex, prepared 24 h after cessation of the chronic ethanol consumption, compared with control values. The results demonstrate that very substantial decreases in firing rate, and in the number of active cells, occur in VTA neurons at a time when withdrawal hyperexcitability was no longer apparent and overt changes in behaviour were not seen.

Action Potentials↗
PubMed1998

Comparison of the effects of drugs on hyperexcitability induced in hippocampal slices by withdrawal from chronic ethanol consumption.

1 The effects of drugs, previously demonstrated to have a range of effects on the behavioural signs of ethanol withdrawal hyperexcitability, were examined in area CA1 in isolated hippocampal slices prepared after withdrawal from chronic ethanol in vivo. 2 The decreases seen after the ethanol treatment in the thresholds for production of single and multiple population spikes were prevented when the dihydropyridine calcium channel antagonist, isradipine, was included in the perfusion medium at 4 microM. 3 Another dihydropyridine, felodipine, which had no activity against withdrawal signs in vivo, did not affect the changes in field potentials, at concentrations up to 10 microM. 4 Diltiazem, which increased withdrawal hyperexcitability in vivo, had no effect on the withdrawal changes in field potentials at 30 microM; higher concentrations affected the control slices. 5 The novel anticonvulsant, gabapentin, at 1 microM but not at 100 nM, significantly decreased the signs of withdrawal hyperexcitability in the hippocampal slices. When the CCKB antagonist, CI988, was added to the bathing medium, at 1 microM, there were small, but significant decreases in the withdrawal hyperexcitability. 6 The results showed that the actions of these drugs on the changes in the field potentials in isolated hippocampal slices were very similar to their previously demonstrated effects on the convulsive signs of ethanol withdrawal in vivo, but differences were seen in the corresponding comparison with anxiolytic actions in vivo.

Acetates↗
PubMed1995

Increases in non-N-methyl-D-aspartate glutamatergic transmission, but no change in gamma-aminobutyric acidB transmission, in CA1 neurons during withdrawal from in vivo chronic ethanol treatment.

Evoked fast excitatory postsynaptic potentials and slow inhibitory postsynaptic potentials were measured in mouse CA1 neurons in hippocampal slices after chronic ethanol treatment in vivo. Intracellular recordings were made 2, 4 and 6 hr after ethanol withdrawal, i.e., after the beginning of slice preparation. The resting membrane potentials were standardized to -60 mV by using constant current injection. The fast excitatory postsynaptic potentials were isolated by adding DL-2-amino-5-phosphonopentanoic acid, bicuculline and nitrendipine to the bathing solution and injecting QX-314 into the recording cell; stimulation then evoked a monophasic depolarization with a maximum of 16.3 mV at about 30 msec after stimulation, which was inhibited by 6-cyano-7-nitroquinozaline-2,3-dione. At 4 and 6 hr after withdrawal, but not at 2 hr, the estimated fast excitatory postsynaptic potential conductance in slices from ethanol-treated mice was significantly larger than in those from control animals. There were no changes in stimulus/response relation or voltage-dependency of the depolarization. In the presence of these blocking agents, the thresholds for elicitation of field potentials was decreased at 6 hr from withdrawal. The slow inhibitory postsynaptic potentials were isolated by adding DL-2-amino-5-phosphonopentanoic acid, 6-cyano-7-nitroquinozaline- 2,3-dione and bicuculline to the bathing solution; stimulation of the Schaffer collateral fibers then evoked a monophasic hyperpolarization with a maximum of 5.7 mV at about 180 msec after stimulation, which was inhibited by the gamma-aminobutyric acidB antagonist saclofen. At the three time points, the stimulus/response relation, voltage dependency of the hyperpolarization and estimated slow inhibitory postsynaptic conductance in ethanol-treated mice did not differ from control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Characterization of the outward rectifying potassium channel in a novel mouse intestinal smooth muscle cell preparation.

1. The outward rectifying K+ conductance and underlying single channel behaviour in mouse small intestine (MSI) smooth muscle cells was studied using microelectrode impalement and the patch clamp technique. 2. At 37 degrees C, smooth muscle cells in MSI explants had a resting membrane potential around -65 mV and showed spontaneous electrical and mechanical activity. 3. Under whole-cell voltage clamp, depolarization of smooth muscle cells in the explants evoked a methoxyverapamil (D600)-sensitive, partially inactivating inward current and a non-inactivating outward current. The outward current was also observed in enzymatically dispersed cells from neonatal mouse small intestine. 4. The reversal potential of the outward current as established in tail current experiments was -70.2 mV. Tail currents could be fitted with a single exponential, suggesting the participation of only one population of channels. 5. The outward current was sensitive to 4-aminopyridine (10(-4) M), Ba2+ (1 mM) and to the presence of Cs+ in the pipette, but not to D600 (10(-6) M), or the presence of ATP (1 mM) in the pipette. 6. In the cell-attached patch configuration, a unitary outward current was observed that showed increased activity upon depolarization of the patch. The current-voltage relationship was close to linear with a slope conductance of 186 pS. 7. With normal K+ (6 mM) in the pipette, the extrapolated reversal potential for the unitary current was around -75 mV, while with high K+ (120 mM) the reversal potential was close to 0 mV. 8. Averaging single channel traces recorded under a depolarizing pulse protocol resulted in a trace with similar time characteristics as the outward current observed in the whole-cell configuration. 9. The burst behaviour of the channel was described by a simple model consisting of two closed states, Cf (intraburst closed state) and Cs (interburst closed state) and an open state (O). The rate constants in the model showed differential sensitivity to potential changes, channel blockade by Ba2+ and equimolar K+ conditions. 10. It was concluded that the outward rectifying potassium current in MSI smooth muscle cells is mediated by a 186 pS bursting channel. Voltage dependency and Ba2+ blockade are mainly reflected by changes in the transition rate from the open channel state to the interburst closed state.

4-Aminopyridine↗
PubMed1992

Intercellular communication in smooth muscle.

The functioning of a group of cells as a tissue depends on intercellular communication; an example is the spread of action potentials through intestinal tissue resulting in synchronized contraction. Recent evidence for cell heterogeneity within smooth muscle tissues has renewed research into cell coupling. Electrical coupling is essential for propagation of action potentials in gastrointestinal smooth muscle. Metabolic coupling may be involved in generation of pacemaker activity. This review deals with the role of cell coupling in tissue function and some of the issues discussed are the relationship between electrical synchronization and gap junctions, metabolic coupling, and the role of interstitial cells of Cajal in coupling.

Animals↗
PubMed1992

Calcium release from separate receptor-specific intracellular stores induced by histamine and ATP in a hamster cell line.

1. The specificity of intracellular Ca2+ stores to Ca(2+)-mobilizing agonists was studied in DDT1 MF-2 vas deferens cells of the Syrian hamster. 2. Application of histamine (100 microM) or ATP (100 microM) to the DDT1 MF-2 cells caused an initial increase of intracellular Ca2+ followed by a lower phase as measured by using Indo-1 as fluorescent probe at 22 degrees C. The basal Ca2+ level (146 nM) was enhanced to 309 nM by histamine and to 379 nM by ATP. 3. A transient rise in intracellular Ca2+ lasting for about 2 min was measured in the presence of histamine or ATP in the absence of extracellular Ca2+. The basal Ca2+ level (78 nM) was increased to 128 nM by histamine and to 145 nM by ATP. 4. A transient hyperpolarization was elicited in single cells as measured with microelectrodes by both agonists under Ca(2+)-free conditions with a similar time course as the change in internal Ca2+. The hyperpolarization observed in the presence of histamine amounted to 23 mV and 31 mV with ATP. The histamine-induced responses were abolished by the H1 histaminoceptor antagonist mepyramine (10 microM) and the responses evoked by ATP were blocked by the P2 purinoceptor antagonist suramin (300 microM). 5. A second internal Ca2+ response could only be evoked under Ca(2+)-free conditions by applying a higher agonist concentration or after replenishing the intracellular stores with Ca2+ from the extracellular space. 6. A second addition of an optimal concentration (100 microM) of the agonist to the cells under Ca(2+)-free conditions did not evoke mobilization of internal Ca2+ or hyperpolarization, but resulted in a rise of the cellular inositol (1,4,5)-trisphosphate content (Ins(1,4,5)P3) as determined by a radioligand binding assay. 7. The cells responded to both agonists (100 microM) with a transient Ca2+ response if successively applied at a maximal effective concentration (100 microM) under Ca(2+)-free conditions. 8. Simultaneous stimulation of H1 histaminoceptors and P2 purinoceptors resulted in the absence of external Ca2+ in an additional increase in internal Ca2+ represented by the amplitude and area of the response and in an increased response area of the hyperpolarization.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1991

Potassium channels regulated by inositol 1,3,4,5-tetrakisphosphate and internal calcium in DDT1 MF-2 smooth muscle cells.

This study was carried out to determine the intracellular components responsible for the transmembrane current evoked by stimulation of H1-histaminergic receptors in DDT1 MF-2 smooth muscle cells. Histamine elicited an outward current that was reversed below the K+ equilibrium potential and passed voltage-independent K+ channels. A histamine concentration-dependent rise in outward current and in cytoplasmic-free Ca2+ with similar time courses was observed. The histamine-induced current was not found after depletion of internal Ca2+ stores, suggesting a coupling between internal Ca2+ and K+ current. The time course of the initial increase in inositol (1,4,5)-trisphosphate (Ins (1,4,5)P3) caused by histamine differs from that of the internal Ca2+ response. However, a significant concentration-dependent increase in inositol (1,3,4,5)-tetrakisphosphate (Ins (1,3,4,5)P4) was seen during the whole stimulating period. The role of internal Ca2+, Ins (1,4,5)P3, and Ins (1,3,4,5)P4 on the outward current was also examined by the addition of these substances directly to the cytoplasm. Internal application of Ca2+ increased the amplitude and duration of the histamine-induced current whereas internal EGTA suppressed the outward current. Internal Ins (1,4,5)P3 did not affect the histamine-induced K+ current, Ins (1,3,4,5)P4 inhibited the outward current, and the combination of Ins (1,3,4,5)P4 and Ca2+ abolished this response. The noradrenaline response evoked under normal conditions is not reflected by a change in transmembrane current or a change in Ins (1,3,4,5)P4 but is associated with an increase in Ins (1,4,5)P3 and internal Ca2+. Stimulation of alpha 1-adrenoceptors, however, also evoked an outward current after the addition of Ins (1,3,4,5)P4 intracellularly. It is concluded that K+ channels, carrying the histamine outward current, are activated from the combined action of internal Ca2+ and Ins (1,3,4,5)P4.

Animals↗
PubMed1991

Voltage-dependent sodium and potassium, but no calcium conductances in DDT1 MF-2 smooth muscle cells.

Voltage-dependent inward and outward membrane currents were investigated in the DDT1 MF-2 smooth muscle cell line using the whole-cell patch-clamp technique. Application of a pulse protocol with subsequent depolarizing voltage steps elicited an inactivating inward current and a non-inactivating outward current. The outward current was activated at membrane potentials more positive than -35 mV, with tau act = 30 -40 ms. The outward current was blocked by tetraethylammonium (NEt4Cl) and 3,4-aminopyridine in a dose-dependent manner (EC50 of 5 mM and 0.5 mM, respectively). The amplitude of the outward current was linked to the potassium equilibrium potential (Vek), and tail currents reversed near Vek. The outward current was completely abolished when intracellular potassium was substituted by 106 mM caesium and 20 mM NEt4Cl. The inward current was activated at potentials more positive than -30 mV with tau act of 1.6-2.5 ms, and with tau inact of 1.7-3.0 ms. Steady-state inactivation was 50% at a holding potential of -40 mV. The inward current was blocked by tetrodotoxin (EC50 of 0.15 microM) and dependent on the reversal potential for sodium. Voltage-dependent calcium currents could not be detected. Further, the cytoplasmic free calcium concentration, as measured using Indo-1 fluorescence, was not changed during high-potassium (40 mM)-induced depolarization. In contrast, contraction of freshly obtained hamster vas deferens tissue elicited by high-potassium(40 mM)-induced depolarization was largely inhibited by diltiazem (20 microM). These findings showed that voltage-dependent calcium channels are not functional in DDT1 MF-2 smooth muscle cells in contrast to freshly obtained Syrian hamster vas deferens smooth muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminopyridines↗
PubMed1990

P2 purinoceptor-mediated inositol phosphate formation in relation to cytoplasmic calcium in DDT1 MF-2 smooth muscle cells.

The effect of P2 purinoceptor stimulation on inositol phosphate (InsP) formation in relation to the intracellular Ca2+ concentration was measured in vas deferens DDT1 MF-2 smooth muscle cells. The different [3H]myo-inositol-labelled InsP fractions were analyzed by high performance liquid chromatography and intracellular Ca2+ was determined by measuring fluorescence using Indo-1 as indicator. Stimulation with ATP (10(-4) M) resulted in an enhanced formation of inositol mono-, bis-, tris- and tetrakisphosphate (InsP1, InsP2, InsP3 and InsP4), but no changes occurred in the formation of inositol pentakis- and hexakisphosphate (InsP5 and InsP6). The putative second messenger Ins(1,3,4,5)P4 rapidly increased after addition of the agonist, reaching a maximum after about 2 min. The isomer Ins(1,4,5)P3 showed a delayed rise starting after about 2 min. The formation of Ins(1,3,4,5)P4 in the presence of ATP (2 min) was concentration-dependent, reaching a half maximal value at about 50 microM of the agonist. The intracellular Ca2+ concentration showed an initial increase after P2 purinoceptor stimulation, reaching a plateau after 2 min. Both the top of the initial phase and the plateau value of the response reached a half maximal value at an ATP concentration of about 7 microM. This Ca2+ response could be evoked repeatedly by ATP and was not affected by diltiazem (10(-5) M). In the absence of external Ca2+, the internal Ca2+ concentration increased transiently in the presence of ATP without showing the plateau phase. This response could be evoked only once under Ca2(+)-free conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1990

Alpha-adrenoceptor regulation of inositol phosphates, internal calcium and membrane current in DDT1 MF-2 smooth muscle cells.

The effect of alpha 1-adrenoceptor stimulation on inositol phosphates (InsPs), intracellular Ca2+ and membrane current was measured in vas deferens DDT1 MF-2 cells. The InsPs were analyzed after labelling the cells with [3H]myo-inositol using high performance liquid chromatography and the internal Ca2+ concentration was determined by measuring fluorescence using Indo-1 as probe. Noradrenaline stimulated the formation of inositol mono-, bis-, tris- and tetrakisphosphate (InsP, InsP2, InsP3 and InsP1) concentration-dependently in the presence of LiCl, but no changes occurred in the formation of inositol pentakis- and hexakisphosphate (InsP5 and InsP6). Various isomers of InsP3 and InsP4 were detected after noradrenaline (10(-5) M) stimulation (without LiCl). Only the formation of the putative second messenger Ins(1,4,5)P3 formation was increased in the presence of noradrenaline. The internal Ca2+ concentration was enhanced both in the presence and absence of external Ca2+ upon addition of noradrenaline. The response in the presence of extracellular Ca2+ was not affected by diltiazem (10(-5) M). The increase in cytoplasmic Ca2+ could be repeatedly evoked, but could be elicited only once under Ca2(+)-free conditions. The relation between the noradrenaline concentration and the rise in internal Ca2+ was similar to that obtained for the InsP formation. Half-maximal effects were obtained at about 1 microM. The membrane current measured in these cells by using the whole-cell patch-clamp method was not changed by the agonist (10(-5) M). These results suggest that noradrenaline acts on DDT1 MF-2 smooth muscle cells, represented by the formation of InsP3 and enhancement of internal Ca2+ originating from internal structures, via the alpha 1B-adrenoceptor subtype.

Animals↗
PubMed1990

P2-purinoceptor-activated membrane currents and inositol tetrakisphosphate formation are blocked by suramin.

The effect of suramin on the ATP-induced response in vas deferens DDT1 MF-2 smooth muscle cells was studied. Stimulation of P2-purinoceptors by ATP caused a change in membrane currents, measured by using the whole-cell patch-clamp configuration, and enhanced the formation of inositol phosphates, as analysed by high performance liquid chromatography. The ATP-induced membrane current consisted of a triphasic response, carried by a fast inward current, followed by a transient outward current and a sustained inward current. Inositol tetrakisphosphate (InsP4) formation increased in the presence of ATP. The formation of the isomers Ins(1,3,4,5)P4, Ins(1,3,4,6)P4 and Ins(3,4,5,6)P4 increased significantly after 5 min stimulation with ATP. Suramin inhibited the ATP-evoked membrane currents and the ATP-induced formation of inositol tetrakisphosphate isomers concentration dependently, but did not affect the basal inositol phosphate levels in the absence of ATP. These results indicate that suramin inhibits ATP-activated cellular processes in DDT1 MF-2 vas deferens cells, most likely by acting on P2-purinoceptors.

Adenosine Triphosphate↗
PubMed1989

P2-purinoceptor-mediated membrane currents in DDT1 MF-2 smooth muscle cells.

The electrophysiological response evoked by ATP was investigated in the DDT1 MF-2 smooth muscle cell line using the microelectrode technique and the whole-cell patch clamp technique. Application of ATP (10(-3) M) to the bathing solution caused a small initial depolarization of the cell membrane, followed by hyperpolarization and slow depolarization. During voltage clamping (-50 mV) a triphasic response was recorded on stimulation with ATP (10(-4)-10(-3) M). A short-lasting inward current was followed by a transient outward current and a slowly decreasing inward current. This response was not affected by the receptor antagonists, propranolol (3 X 10(-6) M), phentolamine (3 X 10(-6) M), atropine (3 X 10(-6) M) or theophylline (10(-3) M). The ATP-induced currents were not modified by the voltage-dependent channel blocking agents, tetraethyl ammonium (3 X 10(-3) M), 3,4-diaminopyridine (10(-3) M), tetrodotoxin (3 X 10(-7) M) or diltiazem (10(-5) M). The fast inward current was not detectable at a low ATP concentration (10(-5) M). The outward current showed a reversal potential near -76 mV, which equals the potassium equilibrium potential. This current was abolished after neutralization of the potassium electrochemical gradient. The outward current was suppressed under calcium-free conditions and also in the presence of tolbutamide (10(-4) M) or glipizide (5 X 10(-6) M). Guanosine triphosphate (5 X 10(-6) M) promoted the outward current, while this current was inhibited in the presence of guanosine diphosphate (5 X 10(-6) M).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗