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J W Deitmer

Publications and source records attributed to J W Deitmer.

At least 19 recordsLinked to original sources
PubMed1992

Evidence for glial control of extracellular pH in the leech central nervous system.

Double-barrelled pH-sensitive microelectrodes were used to measure the intracellular pH (pHi) of neuropil glial cells and the pH of extracellular spaces (pH(e)) within isolated, intact ganglia of the leech Hirudo medicinalis. By application of a weak acid (propionate, 40 mM) or a weak base (ammonium, 20 mM) the total buffer capacity was estimated by changes in glial pHi and in pH(e). The buffering power of glial cells and in the extracellular spaces was increased by up to threefold in the presence of CO2/bicarbonate. The anion exchange inhibitor 4,4-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS, 0.3-0.5 mM) reversed this increase in buffering power both in the glial cells and in the extracellular spaces. Inhibitors of the carbonic anhydrases reduced the CO2/bicarbonate-dependent increase in extracellular buffering power. The results suggest that extracellular H+ buffering dependent upon the availability of bicarbonate is linked to DIDS-sensitive bicarbonate transport across the glial membrane.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1992

Bicarbonate-dependent changes of intracellular sodium and pH in identified leech glial cells.

A new triple-barrelled ion-sensitive microelectrode was used to investigate the importance of bicarbonate for the regulation of intracellular Na+ and pH (Nai and pHi, respectively) of neuropile glial cells in the central nervous system of the leech Hirudo medicinalis. Addition of CO2/HCO3- produced an increase of the Nai activity and an intracellular alkalinization, indicating bicarbonate accumulation in the glial cells. Changes of external pH (from 7.4 to 7.0 and 7.8) produced large and rapid shifts of pHi and Nai and of the membrane potential in the presence, but not in the absence, of bicarbonate. Thus, acid/base transport and Na+ movements across the glial membrane into and out of the cells were accelerated severalfold in CO2/HCO3(-)-buffered saline as compared to a CO2/HCO3(-)-free, HEPES-buffered saline. The results suggest that the electrogenic, reversible, cotransport of Na+ and HCO3- in the glial cell membrane [3,9] can produce significant changes in intraglial pH and Na activity, and can carry a significant fraction of the total Na+ flux across the cell membrane.

Animals↗
PubMed1992

Kainate/glutamate-induced changes in intracellular calcium and pH in leech glial cells.

Kainate evokes a non-desensitizing membrane depolarization in neuropile glial cells of the leech Hirudo medicinalis. We measured membrane potential and intracellular pH, pH(i), using double-barrelled pH-sensitive microelectrodes, and intracellular calcium, Ca2+i, using the change in fluorescence ratio of intracellularly injected fura-2, in these glial cells in situ. 20-50 microM kainate produced a depolarization of 18-28 mV and a decrease of pH(i) by 0.27 +/- 0.07 pH units. Ca2+i increased by 306 +/- 128 nM upon kainate, which could be inhibited by the non-NMDA antagonist CNQX. Glutamate (0.1 mM) also produced a fall in pH(i) and a rise in Ca2+i, which were however, much smaller. Quisqualate and N-methyl-D-aspartate had only small or no effects on membrane potential, pH(i) or Ca2+i. It is concluded that leech neuropile glial cells have a kainate-type glutamate receptor, which mediate significant transients of intracellular H+ and Ca2+.

Animals↗
PubMed1992

Calcium transients in identified leech glial cells in situ evoked by high potassium concentrations and 5-hydroxytryptamine.

We have recorded the fluorescence of Fura-2-loaded, identified glial cells in the neuropile of the central nervous system of the leech Hirudo medicinalis using the ratio of emission at 350 nm excitation to that at 380 nm excitation as an indicator of intracellular Ca2+ concentration ([Ca2+]i). The neuropile glial cells were exposed by mechanically removing the overlying ganglionic capsule and the neuronal cell bodies and were then impaled using a microelectrode under visual control to inject Fura-2 ionophoretically. The resting Ca2+ level was measured using digitonin or Triton to permeabilize the cell membrane at different external concentrations of Ca2+; it was found to vary between 5 and 79 nmol l-1 and averaged 32 +/- 23 nmol l-1 (+/- S.D., N = 7). Raising the external K+ concentration from 4 to 20 mmol l-1 or adding 50 mumol l-1 5-hydroxytryptamine (5-HT) produced a rapid, reversible rise in [Ca2+]i. During prolonged exposure to high [K+] or 5-HT, [Ca2+]i remained high. Upon restoring normal external [K+] or removing 5-HT, [Ca2+]i returned to its initial resting value within 1-2 min. The responses of [Ca2+]i to high [K+] and 5-HT were greatly reduced in nominally Ca(2+)-free saline, suggesting that the [Ca2+]i transients required an influx of Ca2+ into the cells. In the presence of 5-HT, the rise in [Ca2+]i was accompanied by a decrease in the resistance and an increase in the responsiveness to K+ of the glial cell membrane, indicating the existence of a Ca(2+)-dependent K+ conductance elicited by 5-HT.

Animals↗
PubMed1991

Electrogenic sodium-dependent bicarbonate secretion by glial cells of the leech central nervous system.

The ability to move acid/base equivalents across the membrane of identified glial cells was investigated in isolated segmental ganglia of the leech Hirudo medicinalis. The intracellular pH (pHi) of the glial cells was measured with double-barreled, neutral-ligand, ion-sensitive microelectrodes during step changes of the external pH (pHo 7.4-7.0). The rate of intracellular acidification after the decrease in extracellular pH (pHo) was taken as a measure of the rate of acid/base transport across the glial membrane. Taking into account the total intracellular buffering power, the maximum rate of acid/base flux was 0.4 mM/min in CO2/HCO3-free saline, and 3.92 mM/min in the presence of 5% CO2/10 mM HCO-3, suggesting that the acid/base flux was dependent upon HCO3-. The rate of acid influx/base efflux increased both with the external HCO3- concentration and with increasing pHi (and hence HCO3-i). This suggested that the decrease in pHi was due to HCO3- efflux. The rapid decrease of pHi was accompanied by a HCO3--dependent depolarization of the glial membrane from -74 +/- 5 mV (n = 20) to -54 +/- 7 mV (n = 13). Both this depolarization and the rate of intracellular acidification were greatly reduced by the anion exchange inhibitor 4,4-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS; 0.3-0.5 mM), but were not affected by the removal of external Cl-. Reduction of the external Na+ concentration to one-tenth normal affected the rate of intracellular acidification only in the presence of CO2/HCO3-: the rate increased within the first 3-5 min after lowering external Na+; after longer exposures in low external Na+ the rate decreased, presumably due to depletion of intracellular Na+. Amiloride (1 mM), which inhibits the Na+-H+ exchange in these cells, had no effect on the rate of intracellular acidification. The intracellular Na activity (aNai) of the glial cells was measured to be 5.2 +/- 1.0 mM (n = 8) in CO2/HCO3-free saline; aNai increased to 7.3 +/- 2.2 mM (n = 8) after the addition of 5% CO2/24 mM HCO3-. Upon a change in pHo to 7.0 in the presence of CO2/HCO3-, aNai decreased by an average of 2 +/- 1.1 mM (n = 5); in CO2/HCO3--free saline external acidification produced a transient increase in aNai. It is concluded that, in the presence of CO2/HCO3-, the rate of intracellular acidification in glial cells is dominated by an outwardly directed, electrogenic Na+-HCO3-cotransport. Neurons, which do not possess this cotransporter, acidify at much lower rates under similar conditions.(ABSTRACT TRUNCATED AT 400 WORDS)

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

Membrane potential dependence of intracellular pH regulation by identified glial cells in the leech central nervous system.

1. We have measured the intracellular pH (pHi) and membrane potential of identified glial cells in the central nervous system of the leech, Hirudo medicinalis, using double-barrelled pH-sensitive microelectrodes. 2. When extracellular K+ concentration was increased, the glial membrane potential decreased and pHi increased; lowering the extracellular K+ concentration hyperpolarized the glial membrane and decreased pHi. These pHi changes were largely dependent upon the presence of CO2-HCO3-; in nominally CO2-HCO3(-)-free saline solution, they were 50-80% smaller. 3. The steady-state pHi of the glial cells in CO2-HCO3(-)-buffered saline solution strongly correlated with the membrane potential between -40 and -90 mV. The slope of this relationship was 60 mV/pH unit. 4. The neurotransmitter 5-hydroxytryptamine (50 microM), which hyperpolarizes the glial membrane, also produced a large, CO2-HCO3(-)-dependent decrease in pHi. The size of the pHi change depended upon the amplitude of the membrane hyperpolarization. 5. The increase in pHi produced by the membrane depolarization in 20 mM-K+ was abolished in Na(+)-free saline. Removal of external Na+ in the presence of 20 mM-K+ reversed the pHi increase. 6. The pHi increase in 20 mM-K+ was also inhibited by the stilbene 4,4-diisothiocyanostilbene-2'-disulphonic acid (DIDS, 0.5 mM). In a DIDS-poisoned preparation a small decrease of pHi was observed in 20 mM-K+ both in the presence and nominal absence of CO2-HCO3-. 7. In neurones, neither CO2-HCO3- nor 20 mM-K+ produced an intracellular alkanization. The steady-state pHi of several identified neurones was not correlated with the membrane potential. 8. We conclude that in glial cells, but not in neurones, the pHi is dependent upon the membrane potential. This membrane potential dependence is due to the activity of the electrogenic Na(+)-HCO3- co-transporter in the glial cell membrane.

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

An inwardly directed electrogenic sodium-bicarbonate co-transport in leech glial cells.

1. We have used double-barrelled ion-sensitive microelectrodes to measure the intracellular pH, pHi, the intracellular Na+ activity, aiNa, and the membrane potential in identified glial cells of the central nervous system of the leech Hirudo medicinalis to study the effect of CO2-HCO3-. 2. When a HEPES-buffered saline was exchanged for a saline buffered with 2% CO2 + 11 mM-HCO3-, keeping the pH constant at 7.4, the mean steady-state pHi of the glial cells increased from 6.85 +/- 0.06 to 7.18 +/- 0.13 (mean +/- S.D., n = 25). 3. This CO2-HCO3- -dependent alkalinization was inhibited in the absence of external Na+ (exchanged by N-methyl-D-glucamine), but was unaffected by the inhibitor of Na+-H+ exchange, amiloride (2 mM). 4. The aiNa of the glial cells increased by 2-4 mM from a mean steady state of 7.2 +/- 2 mM (mean +/- S.D., n = 6) upon introduction of CO2-HCO3- -buffered saline. This CO2-HCO3- -dependent rise in aiNa increased to about double when the pHi had been decreased by acid loading the cells (addition and subsequent removal of NH4+). 5. The CO2-HCO3- -dependent increases of pHi and aiNa were inhibited by the stilbene 4,4-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS, 0.5-1.0 mM). 6. Removal of external Cl- and depletion of intracellular Cl- did not inhibit the CO2-HCO3- -dependent alkalinization. 7. The CO2-HCO3- -dependent alkalinization was unaffected by inhibitors of the carbonic anhydrase, acetazolamide (0.2 mM) or ethoxzolamide (2 microM). 8. The membrane potential became more negative by 3-20 mV upon addition of CO2-HCO3-. This hyperpolarization was even further enlarged in the presence of Ba2+ (which reduces the K+ permeability) or at increased external K+ concentration (which depolarizes the membrane and brings the membrane potential to the K+ equilibrium potential). The CO2-HCO3- -induced membrane hyperpolarization was inhibited in Na+-free saline and in the presence of DIDS. Ouabain (0.5 mM) sometimes reduced, but never abolished, the hyperpolarization. 9. The stoichiometry of the co-transport is suggested to be 2 HCO3-:1 Na+ with an equilibrium potential of -90 mV calculated for this coupling ratio in the steady state. 10. It is concluded that in the presence of CO2-HCO3- an inwardly directed electrogenic Na+-HCO3- co-transport is stimulated across the glial membrane, which greatly determines the pHi and thereby affects the intracellular buffering power of the glial cells.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1988

Ionic mechanisms of intracellular pH regulation in the nervous system.

Two separate mechanisms responsible for intracellular pH (pHi) regulation in neuronal membranes of the nervous system have been studied so far: they are Na+/H+ and Na+-H+-HCO3-/Cl- exchange. The involvement of these mechanisms in pHi regulation of neurons and glial cells has been investigated in the leech central nervous system using ion-selective microelectrodes. The amiloride-sensitive Na+/H+ exchange is the predominant mechanism of pHi regulation in nominally HCO3- free, Hepes-buffered saline of both neurons and glial cells of this nervous system. In the presence of CO2-HCO3- buffer, however, the SITS-sensitive Na+-H+-HCO3-/Cl- exchanger contributes to acid extrusion in neurons and probably also in glial cells. Unlike neuronal pHi, glial pHi increases when Hepes is replaced by CO2-HCO3- as the extracellular buffer, and decreases again on return to Hepes buffer. The glial alkalinization occurs in the opposite direction, as would be expected from the CO2 movement across the cell membrane and its hydration to form carbonic acid which dissociates into H+ and HCO3- ions. The expected acidification, however, is observed in neurons, and is reduced by acetazolamide and ethoxzolamide, inhibitors of carbonic anhydrase, which catalyses the formation of carbonic acid. On the other hand, these drugs are shown to produce no change of the CO2-HCO3- -induced alkalinization in glial cells. The observations suggest that Na+-HCO3- co-transport across the glial cell membrane, mediating the influx of HCO3- ions into the cell interior, could be responsible for the unusual alkalinization. Further evidence for the activation of Na+-HCO3- co-transport, as a third mechanism involved in pHi homeostasis of the nervous system, is presented.

Acetazolamide↗
PubMed1987

The regulation of intracellular pH by identified glial cells and neurones in the central nervous system of the leech.

1. Double-barrelled, neutral-carrier pH-sensitive micro-electrodes were used to measure the intracellular pH (pHi) and the pHi regulation of neuropile glial (n.g.) cells and of identified neurones of the leech Hirudo medicinalis. 2. The distribution of H+ in the n.g. cells and in the neurones was found not to be in electrical equilibrium. The mean pHi of the n.g. cells was 6.87 +/- 0.13 (mean +/- S.D. of mean here and for all following data n = 27) in HEPES-buffered leech saline (pHo = 7.4) and 7.18 +/- 0.19 (n = 13) in 2% CO2-11 mM-HCO3(-)-saline. The mean pHi was 7.28 +/- 0.1 (n = 20) in Retzius neurones and 7.32 +/- 0.15 (n = 12) in noxious neurones in HEPES-buffered leech saline, and 7.20 +/- 0.15 (n = 10) and 7.27 +/- 0.16 (n = 6) in 2% CO2-11 mM-HCO3(-)-buffered saline in these two types of neurones, respectively. 3. The cytoplasmic buffering power, as calculated by the change in pHi following the change from 2% CO2-11 mM-HCO3- to 5% CO2-22 mM-HCO3- in the leech saline, was 20-30 mM/pH unit in the n.g. cells and between 12 and 33 mM/pH unit in the neurones. 4. The recovery of pHi in n.g. cells from an experimentally induced acidification (addition and removal of 20 mM-NH4Cl) was dependent on the presence of external Na+. Independent of the buffer system used, pHi recovery was inhibited when external Na+ was exchanged by N-methyl-D-glucamine. Amiloride (2-3 mM) reduced the rate of pHi recovery by about 50% in these n.g. cells. 5. In CO2-HCO3(-)-free saline, or in the presence of the anion exchange blocker 4-acetamido-4'-isothiocyanostilbene-2, 2'-disulphonic acid (SITS, 0.5 mM), pHi recovery from an acid load was often slowed by up to 50% in n.g. cells. This suggests that there is a significant contribution of a HCO3(-)-dependent membrane transport to pHi regulation in n.g. cells. 6. When a HEPES-buffered saline was exchanged by a 2% CO2-11 mM-HCO3(-)-buffered saline, the pHi of n.g. cells increased by 0.31 pH units. This alkaline shift was reversible upon removal of the CO2-HCO3- and was absent in the Na+-free saline. It was not inhibited by 1 mM-furosemide or by 0.5 mM-SITS.(ABSTRACT TRUNCATED AT 400 WORDS)

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗
PubMed1986

Inhibition of a voltage-dependent Ca current by concanavalin A.

Incubation of the hypotrichous ciliate Stylonychia mytilus in fluorescein-labeled concanavalin A (Con A, 0.1-0.5 microgram/ml) produced a strong fluorescence of its membranelles, but comparatively weak fluorescence of the other compound cilia and of the somatic membrane. Compared to untreated cells, the frequency of spontaneous backward movements was reduced in the presence of 0.5 microgram/ml ConA. In electrophysiological experiments Con A altered the excitability of the cell membrane. The two-peak action potential lost its second component which is associated with voltage-dependent Ca channels in the membranelles. The corresponding Ca current (Ca current I) was inhibited by low concentrations of Con A (0.2-0.5 microgram/ml). A second voltage-dependent Ca current (Ca current II) was not affected. Reducing the K outward current by intracellular Cs and/or extracellular tetraethylammonium, or changing the holding potential, did not restore the Con A-sensitive Ca current I. Con A also inhibited this current when Ca was replaced by Ba. The inhibitory effect of Con A on the voltage-dependent Ca current I was prevented by 10-30 mM alpha-methyl-D-mannoside, and the lectin wheat germ agglutinin (20 micrograms/ml) did not affect the Ca currents, indicating that the Con A effect was mediated by binding to specific sugar residues on the excitable membrane. The succinylated dimeric derivative of Con A did not inhibit Ca current I up to concentrations of 5 micrograms/ml. It is concluded that the two voltage-dependent Ca currents in Stylonychia can be chemically isolated due to their different sensitivity to Con A, which appears to bind preferentially to sites near or at the Ca channel in the membranellar membrane.

Animals↗
PubMed1986

Changes in voltage-dependent calcium currents during the cell cycle of the ciliate Stylonychia.

Electrophysiological properties of the hypotrichous ciliate Stylonychia mytilus were studied at two stages of its cell cycle: within 30 min after cell division and several hours thereafter. The action potential wave form, and the relative amount of two voltage-dependent calcium inward currents are significantly different in 'young' daughter cells as compared with 'adult' cells. The ratio between total inward and outward current is also larger in 'young' cells. The results provide evidence that during its cell cycle Stylonychia undergoes qualitative developmental changes with respect to its ionic channels in the membrane. These changes may explain the different cell behaviour observed up to 1 h after cell division.

Action Potentials↗
PubMed1986

Single nisoldipine-sensitive calcium channels in smooth muscle cells isolated from rabbit mesenteric artery.

Single smooth muscle cells were enzymatically isolated from the rabbit mesenteric artery. At physiological levels of external Ca, these cells were relaxed and contracted on exposure to norepinephrine, caffeine, or high levels of potassium. The patch-clamp technique was used to measure unitary currents through single channels in the isolated cells. Single channels were selective for divalent cations and exhibited two conductance levels, 8 pS and 15 pS. Both types of channels were voltage-dependent, and channel activity occurred at potentials positive to -40 mV. The activity of both channel types was almost completely inhibited by 50 nM nisoldipine. These channels appear to be the pathways for voltage-dependent Ca influx in vascular smooth muscle and may be the targets of the clinically used dihydropyridines.

Animals↗
PubMed1986

Voltage dependence of two inward currents carried by calcium and barium in the ciliate Stylonychia mytilus.

Two voltage-dependent inward currents in the fresh-water hypotrichous ciliate Stylonychia mytilus have been investigated, using two intracellular micro-electrodes, when either Ca ions or Ba ions are the charge carriers. In cells bathed in Ca-free Ba solution the two inward currents, named current I and current II, could be identified and studied in the absence of outward currents. The two inward currents could also be separated by addition of the plant lectin concanavalin A (0.5 microgram/ml) to the external medium, which resulted in the selective inhibition of current I. When the holding potential was set at values between -45 and -65 mV (normal resting potential is -50 mV), current I was shifted parallel to the holding potential along the voltage axis. This shift was 7.6 mV per 10 mV change in holding potential. The amplitude and voltage relationship of current II was not affected by these changes in the holding potential. The amplitude of current I in Ba solution was maximal when the membrane potential was held at -55 mV; it decreased with higher and lower holding potentials. The rate of activation of current I remained virtually unaffected at holding potentials between -45 and -60 mV, and was somewhat reduced at a holding potential of -65 mV. When the extracellular Ca concentration was varied between 0.1 and 5.0 mM, or when the cells were loaded with EGTA to reduce the intracellular level of ionized Ca, the resting membrane potential and the voltage relationships of both current I and II and of the outward current were shifted along the voltage axis according to the expected changes in membrane surface potential. Double-pulse experiments with varying interval potentials suggested voltage-dependent inactivation of current I and Ca-dependent inactivation of current II. Pre-hyperpolarizing steps of only 1 mV amplitude and 30 ms duration could result in the activation of current I, indicating that the activation voltage of current I closely followed the actual membrane potential. Hence, the same voltage steps elicited similar current I amplitudes with holding potentials between -45 and -60 mV. The results indicate that current II displays voltage properties described for Ca channels in other ciliates and many multicellular preparations, while current I shows an unusual voltage behaviour, which might be regarded as an 'adaptive type of excitation'.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1985

Two components of Ca-dependent potassium current in identified neurons of Aplysia californica.

Outward tail currents measured in Aplysia neurones after termination of depolarizing voltage-clamp pulses consist of rapidly decaying voltage-dependent K currents and slow tail currents of much slower time course. The rapidly decaying voltage-dependent tail currents were blocked with aminopyridines, and measurements of the slow tail currents were made following decay of any residual rapid tail currents. The slow tail current exhibited two components of differing sensitivity to externally applied tetraethylammonium (TEA) ions. In some neurones of the abdominal ganglion (L-2, L-4), virtually all of the slow tail current was resistant to blockage by TEA, while in others (L-3, L-6) 80% or more of the slow tail current was blocked by low TEA concentrations (KD less than 1 mM), the remaining slow tail current being resistant to TEA. This TEA-resistant slow tail current was identified as a K current because it reversed near the K equilibrium potential (EK), the reversal potential was shifted by changes in the external K concentration, and it could be blocked by injection of Cs+. It was abolished by replacement of external Ca2+ by Co2+ or Ba2+, by addition of Cd2+, or by injection of EGTA, and thus determined to be a Ca-dependent current. Intracellular injection of TEA or external application of aminopyridine or apamine had little or no effect on the TEA-resistant slow tail current. Quinidine reduced the TEA-sensitive, but not the TEA-resistant current. Both the TEA-sensitive and the TEA-resistant components of the slow tail current exhibited similar time courses of decay.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1978

Changes in the intracellular sodium activity of sheep heart Purkinje fibres produced by calcium and other divalent cations.

1. The intracellular Na activity of sheep heart Purkinje fibres was recorded with Na+-sensitive glass micro-electrodes. The effects of various external divalent cations on the intracellular Na activity were investigated. 2. Raising the external concentration of divalent cations (Ca, Mg, Mn, Sr or Ba) from 3 to 16 mM resulted in a decrease in the intracellular Na activity of 10-50%. 3. Raising the external concentration of Ca, Sr or Ba could produce a decrease in the intracellular Na activity even when the Na-K pump was inhibited (with strophanthidin, 10(-5) M); but raising the external concentration of Mg or Mn could not. 4. Mn inhibited the decrease in the intracellular Na activity produced by raising external Ca while the Na-K pump was inhibited. 5. Raising external Ca or adding Mn reduced the rate of rise of the intracellular Na activity on inhibition of the Na-K pump. 6. The removal of external K resulted in an increase in the intracellular Na activity. This increase could be stopped and even reversed by raising external Ca. 7. Removal of divalent cations from the external solution produced an increase in the intracellular Na activity. However, replacing external Ca and Mg by another divalent cation, e.g. Mn, did not result in a rise in the intracellular Na activity, except when the Na-K pump was inhibited. 8. The intracellular Na activity decreased by approximately 50% for a tenfold increase in the external Ca concentration. 9. The extent of the decrease in internal Na activity produced by raising external Ca was directly proportional to the internal Na activity before external Ca was raised. 10. We conclude that external Ca influences the intracellular Na activity in two ways: (a) by changing the passive Na influx: the resultant change in the intracellular Na depends on the activity of the Na-K pump; and (b) by a process where internal Na ions are exchanged for external Ca ions.

Animals↗