External Potassium Ion Concentration Research Articles

The Dependence of Auditory Nerve Rate Adaptation on Electric Stimulus Parameters, Electrode Position, and Fiber Diameter: A Computer Model Study

This paper describes results from a stochastic computational neuron model that simulates the effects of rate adaptation on the responses to electrical stimulation in the form of pulse trains. We recently reported results from a single-node computational model that included a novel element that tracks external potassium ion concentration so as to modify membrane voltage and cause adaptation-like responses. Here, we report on an improved version of the model that incorporates the anatomical components of a complete feline auditory nerve fiber (ANF) so that conduction velocity and effects of manipulating the site of excitation can be evaluated. Model results demonstrate rate adaptation and changes in spike amplitude similar to those reported for feline ANFs. Changing the site of excitation from a central to a peripheral axonal site resulted in plausible changes in latency and relative spread (i.e., dynamic range). Also, increasing the distance between a modeled ANF and a stimulus electrode tended to decrease the degree of rate adaptation observed in pulse-train responses. This effect was clearly observed for high-rate (5,000 pulse/s) trains but not low-rate (250 pulse/s) trains. Finally, for relatively short electrode-to-ANF distances, increases in modeled ANF diameter increased the degree of rate adaptation. These results are compared against available feline ANF data, and possible effects of individual parameters are discussed.

Functional Expression of Ion Channels in Mesenchymal Stem Cells Derived from Umbilical Cord Vein

Mesenchymal stem cells have the ability to renew and differentiate into various lineages of mesenchymal tissues. We used undifferentiated human mesenchymal-like stem cells from human umbilical cord vein (hUC-MSCs), a cell line which contains several mesenchymal cell markers. We characterized functional ion channels in cultured hUC-MSCs with whole-cell patch clamp and reverse transcription-polymerase chain reaction (RT-PCR). Three types of outward current were found in these cells: the Ca(2+)-activated K(+) channel (IK(Ca)), a transient outward K(+) current (I(to)), and a delayed rectifier K(+) current (IK(DR)). IK(Ca) and IK(DR) were totally suppressed by tetraethylammonium, and IK(Ca) was sensitive to a specific blocker, iberiotoxin. I(to) was inhibited by 4-aminopyridine. Another type of inward rectifier K(+) current (K(ir)) was also detected in approximately 5% of hUC-MSCs. Elevation of external potassium ion concentration increased the K(ir) current amplitude and positively shifted its reversal potential. In addition, inward Na(+) current (I(Na)) was found in these cells ( approximately 30%); the current was blocked by tetrodotoxin and verapamil. In the RT-PCR analysis, Kv1.1, Kv4.2, Kv1.4, Kir2.1, heag1, MaxiK, hNE-Na, and TWIK-1 were detected. These results suggested that multiple functional ion channel currents, IK(Ca), IK(DR), I(to), I(Na), and K(ir), are expressed in hUC-MSCs. Disclosure of potential conflicts of interest is found at the end of this article.

Triggered alternans in an ionic model of ischemic cardiac ventricular muscle.

It has been known for several decades that electrical alternans occurs during myocardial ischemia in both clinical and experimental work. There are a few reports showing that this alternans can be triggered into existence by a premature ventricular contraction. Detriggering of alternans by a premature ventricular contraction, as well as pause-induced triggering and detriggering, have also been reported. We conduct a search for triggered alternans in an ionic model of ischemic ventricular muscle in which alternans has been described recently: a one-dimensional cable of length 3 cm, containing a central ischemic zone 1 cm long, with 1 cm segments of normal (i.e., nonischemic) tissue at each end. We use a modified form of the Luo-Rudy [Circ. Res. 68, 1501-1526 (1991)] ionic model to represent the ventricular tissue, modeling the effect of ischemia by raising the external potassium ion concentration ([K(+)](o)) in the central ischemic zone. As [K(+)](o) is increased at a fixed pacing cycle length of 400 ms, there is first a transition from 1:1 rhythm to alternans or 2:2 rhythm, and then a transition from 2:2 rhythm to 2:1 block. There is a range of [K(+)](o) over which there is coexistence of 1:1 and 2:2 rhythms, so that dropping a stimulus from the periodic drive train during 1:1 rhythm can result in the conversion of 1:1 to 2:2 rhythm. Within the bistable range, the reverse transition from 2:2 to 1:1 rhythm can be produced by injection of a well-timed extrastimulus. Using a stimulation protocol involving delivery of pre- and post-mature stimuli, we derive a one-dimensional map that captures the salient features of the results of the cable simulations, i.e., the {1:1-->2:2-->2:1} transitions with {1:1<-->2:2} bistability. This map uses a new index of the global activity in the cable, the normalized voltage integral. Finally, we put forth a simple piecewise linear map that replicates the {1:1<-->2:2} bistability observed in the cable simulations and in the normalized voltage integral map. (c) 2002 American Institute of Physics.

Acetylcholine-Induced Vasodilation in the Uterine Vascular Bed of Pregnant Rats with Adriamycin-Induced Nephrosis

Objective: This project was designed to study endothelium-dependent vasodilation in the uterine vascular bed during experimentally induced preeclampsia in rats. Methods: Uterine vascular beds were isolated from nonpregnant and pregnant rats with or without treatment with adriamycin (ADR) and perfused with physiological solution. Thereafter, vasodilator responses to acetylcholine were recorded. Records: Pregnant ADR-treated rats displayed symptoms of preeclampsia including hypertension and proteinuria. Blood pressure was 110.0 ± 4.7 mm Hg (n = 5) in control pregnant rats and 136.0 ± 5.3 mm Hg (n = 5) in ADR-treated pregnant rats, and urinary protein concentrations were 0.35 mg/ml (n = 5) and 13.2 ± 3.6 mg/ml (n = 9), respectively. Both blood pressure and proteinuria values were significantly (p < 0.05) different between controls and ADR-treated rats. However, acetylcholine-induced dose-dependent vasodilator responses in the vascular beds were not significantly different between the pregnant and nonpregnant rats. Although acetylcholine-induced vasodilation was significantly reduced by Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME) in both groups, the residual response to acetylcholine was not affected by indomethacin, suggesting that prostanoids were not involved in this response. The L-NAME-resistant component, endothelium-derived hyperpolarizing factor (EDHF), was greater in ADR-treated uterine beds than in those of the controls, indicating a significant contribution from EDHF in these vessels. In the presence of an elevated external potassium ion concentration, acetylcholine produced similar vasodilator responses, indicating that the release of nitric oxide was not impaired. Conclusion: These results indicate that endothelium-dependent vasodilation was not impaired in this model of preeclampsia.

Galanin Inhibits Continuous and Phasic Firing in Rat Hypothalamic Magnocellular Neurosecretory Cells

The effects of galanin (GAL) on magnocellular neurosecretory cells (MNCs) were examined during microelectrode recordings from supraoptic neurons in superfused hypothalamic explants. Application of the full-length peptide (GAL1-29) or of the N-terminal fragment GAL1-16 produced reversible membrane hyperpolarization with an IC50 near 10 nM. These effects were associated with an increase of membrane conductance, with a reversal potential near -70 mV, and were not blocked by tetrodotoxin, indicating that the receptors mediating these effects are located postsynaptically. Hyperpolarizing responses were also observed in response to the GAL-like chimeric ligands M35 and M40, suggesting that these behave as partial agonists at galanin receptors. The reversal potential of the GAL-mediated effect was unaffected by reducing extracellular chloride or by intracellular chloride injection, indicating that the effects of galanin are not mediated by modulation of chloride conductances. In contrast, reducing the external concentration of potassium ions from 3 to 1 mM shifted the reversal potential of the responses to -85 mV, suggesting the involvement of a potassium conductance. When tested on spontaneously active MNCs, the hyperpolarizing effects of galanin were associated with a suppression of firing in both continuously active and phasically active neurons. Inhibition of phasic bursts was mediated both through the inhibitory effects of the hyperpolarization and through a GAL-mediated inhibition of the depolarizing afterpotential that is responsible for the production of individual bursts. These results suggest that galanin may be a potent endogenous modulator of firing pattern in hypothalamic neuroendocrine cells.

Ion regulation of the kinetics of potential-dependent potassium channels.

We apply a theoretical approach developed earlier. The interaction ofions that permeate a channel with slowly relaxing charged channel-forminggroups (ion-conformational interaction - ICI) is addressed by thisapproach. One can describe the ion concentration influence (ion regulation)on channel functioning in this manner. A patch-clamp method in a'whole-cell' configuration is used to study the ICI. For this purpose theinfluence of an external concentration of potassium ions on thepotential-dependent potassium current (I(A)) in the externalmembrane of GH(3) cells was studied. The increase of[K(+) (out)] from 5 mM to 100 mM causes anon-monotonous shift of current-voltage dependencies. The dependence of bothan activation time constant tgr(n) and a steady-state activation(n(∞)) on [K(+)](out) have a minimum andmaximum respectively. The analysis of the results suggests that the observedeffects are caused by ICI. A physical model is developed to describe thedependence of the potassium channel kinetics on the external concentrationof the ions and the membrane potential. The 'deformation' of the closedstate of the gate and the corresponding energy shifts cause the observednon-monotonous dependencies due to ICI. Thus, the general theoreticalapproach has an experimental confirmation and is applied to concreteexamples. Formulas for concentrational dependencies of the channel kineticsare given for practical uses.

Modulation of inwardly rectifying currents in rat sympathetic neurones by muscarinic receptors.

1. Intracellular recordings were made from rat sympathetic neurones in isolated superior cervical ganglia (SCG), coeliac ganglia (CG), and superior mesenteric ganglia (SMG). 2. Following classification of the firing properties of these neurones as either 'phasic' or 'tonic', single-electrode voltage-clamp recordings of the inwardly rectifying current were performed. The inward rectifier conductance was 6.4 times larger in tonic neurones than in phasic neurones. 3. The basic features of the inward rectifier in sympathetic neurones were similar to those of the classic inward rectifier described in several neuronal and non-neuronal preparations. The properties of the native channel were also similar to a subset of recently cloned inwardly rectifying channels. The reversal potential and the slope conductance were both dependent on external potassium ion concentration. The conductance was blocked by low concentrations of external Ba(2+) and Cs(+) ions. 4. A striking feature of the inward rectifier in sympathetic neurones was its modulation by muscarine. Application of 20 microM muscarine produced a mean 78 +/- 1.4% inhibition of the current. From dose-response curves for muscarine a mean dissociation constant of K(D) = 1.95 +/- 0.2 microM was determined. Schild plot analysis using the competitive antagonists pirenzepine and himbacine indicated that the effect of muscarine was mediated by the M(1) class of muscarinic receptors. 5. The inward rectifier was also inhibited by repetitive nerve stimulation which produced a block of the conductance similar to that seen in response to bath-applied muscarine. The onset of inhibition was relatively slow, 20-30 s, suggesting that it is mediated by a soluble second messenger pathway.

Influence of the external concentration of potassium ions on functioning of voltage-dependent potassium channels in GH3 cells

The patch-clamp technique in a whole-cell configuration was used to study the influence of the external concentration of potassium ions on the characteristics of the voltage-dependent potassium current in the plasma membrane of GH3 cells (a cell line isolated from the rat pituitary body tumor). The [K+] out shift from 5 to 100 mM induced a monotonic increase in potassium current with a constant difference between the testing potential and potassium equilibrium potential. The dependence of an activation time constant, τ n , and a steady-state activation,n∞, of the potassium current on [K+] out is of a distinct non-monotononic character with the extremum at 20 mM. Our experiments and theoretical speculations allow us to suppose that the interaction of potassium ions with slowly relaxing charged channel-forming protein groups induced the observed effects.

Variable tensility of the oral arm plate ligaments of the brittlestar Ophiura ophiura (Echinodermata: Ophiuroidea)

The oral arm plates of the brittlestar Ophiura ophiura L. are connected to lateral arm plates at distal and proximal ligamentous junctions. The distal junction is mobile and is disrupted during arm autotomy; the proximal junction is more rigid and does not participate in autotomy. Aspects of the morphology and mechanical properties of the distal and proximal oral arm plate ligaments have been investigated in order to determine if their tensility is under physiological control. By means of creep tests it was found that elevation of the external potassium (K+) ion concentration causes a decrease in the viscosity of the distal ligament which is either transient or continues until rupture intervenes. In forced vibration tests the distal ligament often shows a biphasic stiffening then softening response to excess K ‐ ions. Anaesthetics block the softening phase but enhance the stiffening component of this response. This ligament is also softened by repetitive electrical stimuli but stiffened by excess calcium ions and by acetylcholine. The proximal ligament appears to have the capacity for only transient changes in mechanical properties. Both ligaments are penetrated by the processes of juxtaligamental cells whose perikarya are arranged in clusters innervated by hyponeural nerves. These cells are thought to modulate the interfibrillar cohesion of the ligaments. It is concluded that the distal and proximal ligaments are mutable collagenous structures which in their stiffened condition help to maintain arm posture without the need for continuous muscular activity, and that at autotomy the distal ligament undergoes a profound loss of tensile strength which facilitates arm detachment.

Time‐dependent changes in protein phosphorylation patterns in rat brain synaptosomes caused by deltamethrin

AbstractEffects of deltamethrin, a powerful pyrethroid insecticide, on the protein phosphorylation and dephosphorylation processes during depolarization in rat brain synaptosomes were studied by using [32P]phosphoric acid as a starting radiotracer and high external concentration of potassium ions or veratridine (10−‐5 M) as depolarizing agents. At the onset of depolarization there was a quick rise in phosphorylation in various synaptic proteins for about 15–30 s followed by a gradual decline in levels of phosphorylation. The effect of deltamethrin (10−‐7 M) on this system was found to be dependent on the length of preincubation of the synaptosome with the pesticide prior to depolarization. At an early stage (0–3 min preincubation period) it caused a modest suppression of protein phosphorylation activities. When the period of deltamethrin preincubation was extended to 5–20 min, however, it caused a significant increase in protein phosphorylation throughout the depolarization period. At the later stage of the action of deltamethrin (e.g. preincubation period of 30–40 min), deltamethrin‐treated synaptosomes no longer responded to the depolarization signal to raise the level of phosphorylation on many proteins. These results indicate that deltamethrin's actions on the synaptic process are complex. Depending on the length of exposure, its effects on protein phosphorylation responses in intact synaptosomes could be either stimulatory or inhibitory. To study the cause of deltamethrin‐induced synaptic block at the later stage, effects of deltamethrin on protein kinases were studied by using lysed synaptic membranes with [gamma‐32P]ATP. Deltamethrin was shown to inhibit calcium–calmodulin‐dependent protein phosphorylation activities at 10−‐7 M when given directly to the enzyme source 10 min prior to the addition of [32P]ATP. Such an observation helps to explain the inhibitory action of deltamethrin on protein phosphorylation which occurs at the late stage of its action (i.e. preincubation time &gt; 20 min).

A paradox concerning ion permeation of the delayed rectifier potassium ion channel in squid giant axons.

1. The fully activated current-voltage relation (I-V) of the delayed rectifier potassium ion channel in squid giant axons has a non-linear dependence upon the driving force, V-EK, as I have previously demonstrated, where V is membrane potential and EK is the equilibrium potential for potassium ions. 2. The non-linearity of the I-V relation and its dependence upon external potassium ion concentration are both well described, phenomenologically, by the Goldman-Hodgkin-Katz (GHK) flux equation, as I have also previously demonstrated. As illustrated below, this result can be modelled using the Eyring rate theory of single-file diffusion of ions through a channel in the low-occupancy limit of the theory. 3. The GHK equation analysis and the low-occupancy limit of the Eyring rate theory are both consistent with the independence principle for movement of ions through the channel, which is at odds with tracer flux ratio results from the delayed rectifier, published elsewhere. Those results suggest that the channel is multiply occupied by two, or perhaps three, ions. 4. The resolution of this paradox is provided by a triple-binding site, multiple-occupancy model in which only one vacancy, at most, is allowed in the channel. This model predicts current-voltage relations which are consistent with the data (and with the phenomenological prediction of the GHK flux equation). The model is also consistent, approximately, with the tracer flux ratio results.

Determination of the membrane potential of cultured mammalian schwann cells and its sensitivity to potassium using a thiocarbocyanine fluorescent dye

The membrane potential of cultured rat sciatic nerve Schwann cells was determined with conventional microelectrode and voltage-sensitive fluorescent dye, Di-S-C3(5), optical techniques. The value for membrane potential obtained with microelectrodes was -42.1 +/- 4.7 mV (n = 8). Using optically determined fluorescent intensity changes caused by changes in external potassium ion concentration, in the presence or absence of valinomycin (null point method), the membrane potential was estimated at -45.7 +/- 6.2 mV (n = 7); with a gramicidin and valinomycin double ionophore method it was -52.2 +/- 9.1 (n = 4). The membrane potential of Schwann cells was found to be potassium sensitive at and above the physiological range of [K+] at 27.5 mV/10x delta[K+], which is approximately half the Nernstian value. This result suggests that other ion permeabilities strongly influence the resting membrane potential of cultured Schwann cells. Since Na+ had little effect on the membrane potential, it is concluded that Cl- is a likely candidate for the other permeant ionic species. The optical method has been shown to be a useful tool for the systematic study of the membrane potential of Schwann cells in culture and for the characterization of its ionic basis and regulation.

Release of Immunoreactive Insulin from Rat Brain Synaptosomes Under Depolarizing Conditions

Synaptosome preparations were utilized to characterize the release and compartmentalization of immunoreactive insulin (IRI) in the adult rat brain. Depolarization of synaptosomes by elevation of the external potassium ion concentration elicited release of IRI from the synaptosomes into the incubation medium. This release was reduced or eliminated under three conditions known to prevent depolarization-induced Ca2+ flux: elevating the external MgCl2, adding CoCl2, and eliminating external Ca2+ with EGTA. Depolarization of synaptosomes by veratridine also elicited release of synaptosomal IRI. This release was inhibited by tetrodotoxin. The amount of IRI released under depolarizing conditions represented 3-7% of that contained in the synaptosomes. High levels of IRI release also were observed upon removal of external Na+ to allow depolarization-independent influx of external Ca2+ into the synaptosomal compartment. The Ca2+ dependency of synaptosomal IRI release suggests IRI is stored in the adult rat brain in synaptic vesicles within nerve endings from which it can be mobilized by exocytosis in association with neural activity.

Actions of the GABAB agonist, (-)-baclofen, on neurones in deep dorsal horn of the rat spinal cord in vitro.

1. The electrophysiological actions of the GABAB agonist, (-)-baclofen, on deep dorsal horn neurones were studied using an in vitro preparation of the spinal cord of 9-16 day old rat. 2. On all neurones tested, (-)-baclofen (100 nM-30 microM) had a hyperpolarizing action which was associated with a reduction in apparent membrane input resistance. The increase in membrane conductance was dose-dependent and had a Hill coefficient of 1.0. 3. The (-)-baclofen-activated hyperpolarization persisted in the presence of bicuculline (50 microM) and Mg2+ (20 mM). 4. The reversal potential of the hyperpolarizing event was estimated at 102 mV and was made less negative by increasing the external concentration of potassium ions. 5. Over the same concentration range, (-)-baclofen also depressed the polysynaptic composite excitatory postsynaptic potentials (e.p.s.ps) evoked in these neurones by electrical stimulation of the dorsal root entry zone. 6. The potassium channel blockers caesium, applied intracellularly, and barium, applied extracellularly, depressed the postsynaptic response to baclofen but not its effect on e.p.s.ps. 7. We propose that (-)-baclofen has more than one mechanism of action in spinal dorsal horn: a postsynaptic action mediated via an increase in potassium conductance and a presynaptic action that is not associated with potassium channels and may be mediated via calcium channels. Since previous studies have demonstrated little effect of (-)-baclofen on transmitter release in spinal cord, it is possible that the postsynaptic hyperpolarizing action of (-)-baclofen may account for its clinical potency as an anti-spastic agent.

Modulation of a subthreshold calcium current by the neuropeptide FMRFamide in Aplysia neuron R15.

1. The effect of the endogenous neuropeptide FMRFamide (Phe-Met-Arg-Phe-amide) on the Aplysia bursting pacemaker neuron R15 was studied. Brief local applications of FMRFamide, both on R15 somata in situ, and on R15 somata that were isolated and maintained in primary cell culture, cause a hyperpolarization of the membrane potential and a suppression of spontaneous bursting or beating pacemaker activity. 2. Two-electrode voltage-clamp experiments revealed that FMRFamide decreases the amplitude of an inward current, which activates with depolarization starting at a membrane potential less depolarized than the threshold for action potentials. Previous studies have established that this subthreshold inward current is carried by calcium and is essential for the generation of bursting pacemaker activity in Aplysia neurons. The effect of FMRFamide on the subthreshold inward current of R15 is blocked by divalent cation calcium channel blockers, such as cobalt and manganese, and is unaffected by changing the external concentration of potassium or chloride ions, or addition of blockers of the calcium-activated potassium current, such as external tetraethylammonium or internal EGTA. 3. The subthreshold calcium current of R15 is also decreased by dopamine and by an unidentified synaptic neurotransmitter. These substances mimic and occlude the action of FMRFamide on the subthreshold calcium current, suggesting that all three transmitters converge to affect the same population of calcium channels in neuron R15. 4. The subthreshold calcium current is enhanced by neurotransmitters that elevate cyclic AMP in R15, including serotonin, and the Aplysia neuropeptide egg-laying hormone (ELH). Likewise, the effect of FMRFamide on the subthreshold calcium current is enhanced by serotonin, ELH, and a cyclic AMP analog, suggesting that FMRFamide and cyclic AMP have antagonistic actions on the same population of calcium channels in neuron R15. 5. We conclude that the suppression of spontaneous bursting or beating pacemaker activity in neuron R15 by FMRFamide is due to a decrease in the subthreshold calcium current. The subthreshold calcium current in R15 is a common target for modulation by many different transmitters, acting via several distinct molecular mechanisms.

Inward rectification in submucosal arterioles of guinea‐pig ileum.

1. The current-voltage relationships of short segments of submucosal arteriole of guinea-pig have been determined using constant current and voltage clamp techniques. 2. The current-voltage relationships were non-linear over the membrane potential range -60 to -90 mV, the conductance increasing with hyperpolarization. 3. The membrane potential ranges over which the membrane conductance increased were changed by changing the external concentration of potassium ions. 4. Changing the external concentrations of sodium and chloride ions had no effect on the arteriolar current-voltage relationships. 5. The hyperpolarization-activated conductance increase was prevented by low concentrations of barium ions. 6. It is suggested that these arterioles display potassium-selective inward rectification and that the rectifier supplies the dominant resting potassium conductance. The properties of this rectifier are compared with those of other tissues.

Effects of alpha-aminoadipic acid on the glutamate-isolated P III of the rabbit electroretinogram.

alpha-Aminoadipic acid was intravitreally applied to adult rabbits. After 5 h, the retinae of these animals were examined by electroretinography and histochemistry. The retinal Müller cells were extremely swollen, and the electroretinographic slow P III was extinguished. The mass receptor potential was somewhat diminished. The results are consistent with the opinion that the slow P III is the reaction of the Müller cells to the changed external potassium ion concentration caused by the activity of the photoreceptors.

The use of carotenoids and oxonol VI as probes for membrane potential in proteoliposomes

Carotenoids present in lipids extracted from the cyanobacterium Synechococcus 6716 indicate trans-membrane potential in proteoliposomes reconstituted from these lipids and the ATPase complex isolated from the same organism. A carotenoid absorbance band shift to a longer wavelenght is obtained with valinomycin-induced potassium ion diffusion potentials, irrespective of the polarity of the potassium gradient. In contrast to this, the (externally added) probe oxonol VI only shows an absorbance band shift when the external potassium ion concentration is higher than the internal one. In liposomes without ATPase complex, no carotenoid absorbance band shifts were observed.

Zur Interpretation von Membranpotential-Konzentrationsbeziehungen in Pflanzenzellen

According to the Hodgkin-Horowicz equation originally derived from an electrical analogues of the membrane, the potential drop Δ E induced by a sudden change of the external potassium ion concentration Δ K should be linear with respect to the concentration term In(l + Δ K/K01). Analyzing 24 experimental investigations taken from the literature we found that in most cases the above relation does not hold. Taking into account the ionic strength of the medium a modified voltage-concentration relation is derived containing besides others the transport number TK of the Hodgkin-Horowicz equation. All the data taken from the literature agree very well with this modified relation. Some consequences and predictions are discussed.

Ionic basis of the resting potential of submucosal arterioles in the ileum of the guinea-pig.

1. The changes in the resting membrane potential of arterioles produced by rapid and brief changes in external ionic concentrations were measured. 2. The resting membrane potential was insensitive to changes in the external concentrations of both sodium and chloride ions but sensitive to changes in the external concentration of potassium ions. 3. Increasing the external concentrations of potassium ions produced depolarizations that were well described by the Nernst equation. 4. Decreased external concentrations of potassium ions produced membrane depolarizations which appeared to result not from inhibition of an electrogenic sodium pump but rather from a change in the resting conductance of the arteriolar membrane to potassium ions. 5. Ouabain caused both membrane depolarization and an increase in membrane resistance. 6. It is suggested that at rest, arteriolar smooth muscle is permeant predominantly to potassium ions, with only small contributions from chloride and sodium ions. No evidence was obtained which would support the idea that an appreciable proportion of the resting membrane potential depended upon current flow from an electrogenic sodium pump.