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C M Baumgarten

Publications and source records attributed to C M Baumgarten.

49 records · Page 3Linked to original sources
PubMed1985

Intracellular Cl activity changes of frog skin.

The intracellular Cl activity and potential were determined in short-circuited frog skin with single-barrel microelectrodes. With NaCl Ringer solution on the apical and basolateral side, the intracellular Cl activity was 15.5 +/- 0.5 mM and the intracellular potential was -90 +/- 1.0 mV, indicating that the intracellular Cl activity was above electrochemical equilibrium. When the solution on the apical side was changed to a Cl-free solution (Cl replaced by methanesulfonate), no significant difference was observed in intracellular Cl activity. However, when the skins were Cl-depleted by replacing the NaCl Ringer solution on both sides with a Cl-free solution, the intracellular Cl activity decreased to 1.7 +/- 0.1 mM and the intracellular potential fell to -66.7 +/- 1.3 mV. Addition of Cl (i.e., NaCl Ringer solution) to the apical side of Cl-depleted skins caused a significant increase in intracellular Cl activity to 6.3 mM. This increase was prevented by amiloride (10(-4) M) added on the apical side simultaneously with Cl. Restoration of Cl on the basolateral side of Cl-depleted tissues also raised the intracellular Cl activity to about the same level as when Cl was added on the apical side (6.8 mM). Changes in membrane potential occurred in a delayed fashion over a period of 15 min or more when Cl was added or removed on either side of the skin. The absence of an immediate membrane potential response indicates that Cl conductance is not detectable. We conclude, therefore, that the Cl transfer across the apical and basolateral cell membrane occurs primarily via electroneutral mechanisms.

Amiloride↗
PubMed1984

Potential and K+ activity in skinned muscle fibers. Evidence against a simple Donnan equilibrium.

It has been suggested that potentials measured with conventional microelectrodes in chemically or mechanically skinned muscle fibers arise from a Donnan equilibrium due to myofilament fixed charges. This hypothesis was tested in mechanically skinned frog (Rana pipiens) semitendinosus fibers by measuring the distribution potential (Ed) between fiber and bath with 3 M KCl-filled microelectrodes and the K+ activity gradient (aik/aok) with K+ ion-selective microelectrodes (KISE). If skinned fibers are a Donnan system, Ed should become more positive as pH is decreased, altering the fixed charge on the myofilaments. Consistent with this expectation, Ed was -4.4, -0.6, and +4.8 mV in ATP-containing solutions and -6.5, -2.2, and +8.4 mV in ATP-free solutions at pH 7, 6, and 5, respectively. Donnan equilibrium also requires that all mobile ionic species be in electrochemical equilibrium. In ATP-containing solutions, this was true for K+ at pH 7. At pH 5, however, KISE indicated that K+ was not in equilibrium; average Ed was 5.9 mV positive to the K+ equilibrium potential, and aik/aok was 1.04, while the Donnan prediction was 0.83. In contrast, KISE measurements in ATP-free solutions indicated that K+ was in equilibrium at all pH studied. Skinned fibers in ATP-containing media are not equilibrium systems because ATPase reactions occur. Under our conditions, frog myofibrils hydrolyze 0.4 and 0.08 mumol ATP/min X mg myofibrillar protein at pH 7 and 5, respectively. It is suggested that in the presence of ATP, Ed is a superposition of Donnan and diffusion potentials, the latter arising from differences in the mobilities of anionic substrate and products that diffuse through the charged myofilament lattice. A coupling to diffusion of K+, the predominant counter ion, is required for macroscopic electroneutrality. This coupling may be the origin of the nonequilibrium K+ distribution.

Adenosine Triphosphatases↗
PubMed1984

Intra- and extracellular potassium activities, acetylcholine and resting potential in guinea pig atria.

Intracellular potassium activity in guinea pig left atria was measured using potassium ion-selective microelectrodes and conventional microelectrodes. The effects of extracellular potassium concentration and acetylcholine on both intracellular potassium activity and the relationship between the resting membrane potential and the potassium equilibrium potential were investigated. Intracellular potassium activity was 102.1 mM in bathing media with a potassium concentration of 5 mM. Neither increasing extracellular potassium concentration to 10 mM nor exposure to acetylcholine (2 x 10(-6) to 10(-3) M) significantly altered intracellular potassium activity. In contrast, intracellular potassium activity decreased to 92.9 mM in 2.5 mM potassium concentration solutions. Resting membrane potential was 18.6, 9.6, and 7.3 mV positive to the potassium equilibrium potential in 2.5, 5, and 10 mM potassium, respectively. Acetylcholine caused a significant hyperpolarization at each extracellular potassium activity, confirming that resting membrane potential was positive to the potassium equilibrium potential. Even after exposure to 10(-3) M acetylcholine, the resting membrane potential apparently remained positive to the potassium equilibrium potential. If potassium accumulates in extracellular clefts during acetylcholine exposure, the calculated potassium equilibrium potentials are too negative, and the resting membrane potential might closely approximate the potassium equilibrium potential under these conditions. Fading of the acetylcholine-induced hyperpolarization and overshoot of the resting membrane potential on washout of acetylcholine were observed and are consistent with an accumulation of potassium during exposure to acetylcholine. In 5.0 mM potassium bathing solution, preparation-to-preparation variability of resting membrane potential can largely be explained by variability of intracellular potassium activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1981

Intracellular chloride activity in mammalian ventricular muscle.

The intracellular chloride activity (formula, see text) of quiescent rabbit right papillary muscle was measured with ion-selective microelectrodes (ISE) made with Corning 477315 liquid ion-exchange resin. The (formula, see text) was 9.8 +/- 2.4 (SD) mM, a value significantly greater than the 6.1 +/- 0.6 mM expected from passive distribution. The chloride equilibrium potential (ECl) was -64.4 +/- 6.6 mV, while membrane potential was -75.9 +/- 2.2 mV and significantly negative to ECl. These values are corrected for a nonchloride signal detected by the ISE. An apparent (formula, see text) of 4.8 +/- 0.6 mM was measured after exposure to Cl-free media for 1 h. Since isotopic chloride was totally washed out by this time, the apparent (formula, see text) in Cl-free media was interpreted as interference and subtracted from the (formula, see text) measured in other media. The conclusion that chloride is not passively distributed is supported by the observation that the (formula, see text) increase in high potassium media was smaller than predicted. In contrast to findings in papillary muscle, (formula, see text) of frog sartorius muscle was consistent with passive distribution, if it is assumed that interference was less than 0.5 mM.

Animals↗
PubMed1981

An improved liquid ion exchanger for chloride ion-selective microelectrodes.

A new chloride liquid ion exchanger, Corning 477913, suitable for fabricating ion-selective microelectrodes (ISE) is described. It differs from the standard chloride exchanger. Corning 477315, in that the concentration of organophilic ligand is increased fivefold. The properties of ISE (tip diameter less than 1 micrometer) made from the new material are superior to those of ISE made from the standard material. The yield of acceptable ISE was greater (77 vs. 34%); the ISE resistance was decreased 5.3-fold; the average slope was improved (-52.8 vs. -45.5 mV); and the selectivity over some interfering anions was increased. Measurement of intracellular chloride activity in rabbit ventricle with ISE made from the new exchanger gave results similar to those reported previously with the standard exchanger. This suggests that 477913 is satisfactory for use in biological tissue. The new formulation should be particularly advantageous for measurements requiring ISE with very fine tips and in fabrication of multibarrel ISE.

Anions↗
PubMed1981

Heterogeneity of intracellular potassium activity and membrane potential in hypoxic guinea pig ventricle.

The relationship between membrane potential (Em) and the potassium equilibrium potential (EK) was investigated in hypoxic guinea pig papillary muscle. After more than 8 hours of hypoxia, cells with near normal Em (-86.2 +/- 0.9 mV) and action potentials were observed. However, the intracellular potassium concentration ([K+]i) based on chemical analysis and the assumption that potassium was homogeneously distributed was 41.8 +/- 4.3 mM; the apparent EK was -55.7 +/- 2.9 mV, significantly positive to Em. Measurements with potassium ion-selective microelectrodes revealed that prolonged hypoxia results in at least two populations of cells with different characteristics. The first population had an intracellular potassium activity (aiK) of 101.5 +/- 1.9 mM, and EK was 4.7 mV negative to Em. In contrast, EK was 33.4 +/- 1.3 mV negative to Em in the second population. These cells also exhibited a reduced sensitivity to changes in bath potassium, and calculations suggest aiK was about 18 mM. The existence of cell populations with a near normal and very low aiK can explain the intermediate value of [K+]i calculated assuming a homogenous potassium distribution. Cells with near normal Em and action potentials represent the population with near normal aiK. Hypoxia may also cause non-uniform changes in other cellular characteristics.

Animals↗
PubMed1977

Depletion and accumulation of potassium in the extracellular clefts of cardiac Purkinje fibers during voltage clamp hyperpolarization and depolarization.

1. Voltage clamp hyperpolarization and depolarization elicited current records consistent with depletion and accumulation, respectively, of potassium in the extracellular clefts of cardiac Purkinje fibers. Hyperpolarization was shown to shift the reversal potential for the pacemaker current, ik2, a measure of Ek, to more negative potentials. Upon depolarization, a slowly increasing outward current was observed. Analysis of the tail currents elicited by hyperpolarization revealed that a time-dependent change in gx could not explain the time-dependent outward current. However, the tail currents were consistent with a shift of Ek to more positive potentials during the depolarization. 2. Alteration in potassium driving force over time results in a time-dependent ik1 even though the underlying conductance is time-independent [29]. This time-dependent current may contribute to the currents usually identified as ik2 and ix. 3. The potential at which ik2 reverses direction is altered by the clamp program used to elicit it and is obscured by the superimposition of a time-dependent current due to depletion. 4. Records consistent with the extracellular cleft potassium concentration being less than that of the bulk phase in the quiescent fiber were obtained. However, an unequivocal interpretation of these current reocrds could not be made. 5. These results suggest that conclusions based on the assumption that potassium driving force remains constant during a voltage clamp pulse may be in error. Thus, time-dependent currents cannot be assumed to result solely from time-dependent conductance changes.

Animals↗
PubMed1977

Depletion and accumulation of potassium in the extracellular clefts of cardiac Purkinje fibers during voltage clamp hyperpolarization and depolarization: experiments in sodium-free bathing media.

Voltage clamp hyperpolarization and depolarization result in currents consistent with depletion and accumulation of potassium in the extracellular clefts o cardiac Purkinje fibers exposed to sodium-free solutions. Upon hyperpolarization, an inward current that decreased with time (id) was observed. The time course of tail currents could not be explained by a conductance exhibiting voltage-dependent kinetics. The effect of exposure to cesium, changes in bathing media potassium concentration and osmolarity, and the behavior of membrane potential after hyperpolarizing pulses are all consistent with depletion of potassium upon hyperpolarization. A declining outward current was observed upon depolarization. Increasing the bathing media potassium concentration reduced the magnitude of this current. After voltage clamp depolarizations, membrane potential transiently became more positive. These findings suggest that accumulation of potassium occurs upon depolarization. The results indicate that changes in ionic driving force may be easily and rapidly induced. Consequently, conclusions based on the assumption that driving force remains constant during the course of a voltage step may be in error.

Animals↗
PubMed1975

Effect of beta receptor blockade on the initiation and perpetuation of ouabain-induced ventricular tachyarrhythmia.

The role of the cardiac beta receptor in the genesis and perpetuation of ouabain-induced ventricular tachyarrhythmias (VT) was investigated in the chloralose (20 mg/kg)-urethane (200 mg/kg) anesthetized dog. This was achieved by determining: 1) the effect of oxprenolol (0.3 mg/kg), a potent beta receptor blocking agent possessing no significant direct membrane effects on the myocardium, on the dose of ouabain necessary to cause VT (i.e., the toxic dose); and 2) whether oxprenolol had antirrhythmic efficacy against preexisting VT. The toxic dose was determined by giving a bolus injection of ouabain (similar to 36 mug/kg) plus a subsequent ouabain infusion (similar to 0.40 mug/kg min-minus 1) until VT occurred. VT was defined as at least one-third of the ventricular beats being of ectopic ventricular origin. The existence of an effective beta receptor blockade was verified by showing that 0.75 mug/kg of isoproterenol (an ED50 dose) injected intravenously had no detectable cardiovascular effects. The results were: 1) oxprenolol (0.3 mg/kg) did not alter the toxic dose significantly (P greater than .5 for both paired and group comparisons) [63.9 plus or minus 2.3 (S.E.) mug/kg vs. 64.4 plus or minus 2.9 (S.E.) mug/kg]; and 2) attempts to convert VT to sinus rhythm with oxprenolol (0.3 mg/kg) failed in 20 of 21 trials. Oxprenolol (1.0 mg/kg) effected only a temporary [10.6 plus or minus 6.4 (S.D.) minutes] reversion to sinus rhythm in 10 of 21 attempts. These results indicate that an activation of the cardiac beta receptor is not prerequisite for either the initiation or the perpetuation of ouabain-induced ventricular tachyarrhythmia in this particular model. The results cannot provide support for the notion that an increase in cardiac sympathetic nerve activity is a principal factor in VT in the dog. However, the results are consistent with the hypothesis that the direct membrane actions of ouabain are a principal cause of ouabain-induced ventricular tachyarrhythmia.

Adrenergic beta-Antagonists↗