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D Erlij

Publications and source records attributed to D Erlij.

At least 37 records · Page 2Linked to original sources
PubMed1988

Cation-selective channels in amphibian epithelia: electrophysiological properties and activation.

1. Na+ as well as Li+ move across the apical membrane through amiloride-sensitive ionic channels. 2. K+ movements across the apical membrane occur through Ba2+- and Cs+-sensitive channels which do not allow the passage of Na+ or Li+. 3. A third pathway in the apical membrane is permeable for Na+, K+, Cs+, Rb+, NH+4 and Ti+. The currents carried by these monovalent cations are blocked by Ca2+ and divalent cations as well as La3+. 4. In the urinary bladder, the Ca2+-sensitive currents are stimulated by oxytocin, activators of cytosolic cAMP and cAMP analogues. Also the oxytocin activated currents are blocked by divalent cations and La3+. 5. Nanomolar concentrations of mucosal Ag+ activate the third channel and open the pathway for movements of Ca2+, Ba2+ and Mg2+, which are known to permeate through Ca2+ channels in excitable tissues.

Animals↗
PubMed1988

Activation and blockage of a calcium-sensitive cation-selective pathway in the apical membrane of toad urinary bladder.

1. The properties of cation movements through a previously described Ca2+-sensitive oxytocin-stimulated pathway in the apical membrane of the toad urinary bladder were further investigated. 2. In the absence of Ca2+ and other polyvalent cations in the mucosal medium, oxytocin markedly stimulated the flow of current from mucosa to serosa when the major cation in the mucosal solution was any of the following ions: Na+, K+, Rb+, Cs+ or Li+. Analysis of the current noise showed a Lorentzian component associated with the movement of these cations. 3. Ca2+ and other divalent cations in the mucosal solution depressed both the current and the Lorentzian component of the fluctuation spectra. The Michaelis-Menten constants were 2.5, 10 and 58 mumol/l for Ca2+, Sr2+ and Mg2+ respectively. 4. The dihydropyridine Ca2+ channel blockers nitrendipine (10(-5) mol/l) and nicardipine (10(-6) mol/l) inhibited the Ca2+-sensitive current. 5. Alterations of the mucosal pH showed that the current and the plateau of the Lorentzian component increased by elevating the pH from 6 to 8. The Ca2+-sensitive current was further stimulated by increasing pH to 9. However, this manoeuvre resulted in the disappearance of the Lorentzian component in the noise spectrum. 6. Increasing either mucosal [Na+] or [K+] up to 115 mmol/l did not lead to saturation of the current passing through the Ca2+-sensitive channel. In contrast the amiloride-sensitive channel showed saturating behaviour when mucosal [Na+] was increased; half-maximum current was reached when mucosal [Na+] was about 15 mmol/l. 7. When a Na+-free mucosal solution, prepared with either choline or TEA as major cation, was rapidly replaced by a solution with Na+ (115 mmol/l), the current through the Ca2+-sensitive channel increased rapidly and then remained at a nearly constant level. This behaviour is in contrast with the response of the current through the amiloride-sensitive pathway. After suddenly increasing mucosal Na+ concentration ([Na+]m), the current through this channel first increased rapidly and then declined to values of nearly 50% of the peak about 10 min after the increase in [Na+]m.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Activation of K+ conductance in basolateral membrane of toad urinary bladder by oxytocin and cAMP.

We incubated toad urinary bladders with Na+-free, isotonic K+ solutions on the apical side and increased the cationic conductance of the apical membrane with nystatin (150 U/ml). Under these conditions, the short-circuit current is mostly carried by K+ flowing from mucosa to serosa. Impedance measurements showed that in nystatin-treated preparations, the electrical behavior of the tissue is dominated by the basolateral membrane properties. Oxytocin (0.1 U/ml) produced an increase of the current and the conductance of the basolateral membrane. Both the resting and the oxytocin-stimulated current were rapidly and reversibly blocked by serosal Ba2+. Addition of the adenosine 3',5'-cyclic monophosphate (cAMP) analogue [8-(4-chloropheylthio)-cAMP] to the basolateral solution mimicked the effects of oxytocin. These results show that oxytocin and cAMP stimulate a potassium conductance in the basolateral membrane and that the stimulation is not related to an increase in sodium entry through the apical membrane. Addition of ouabain (10(-3) M) to the serosal solution did not modify the stimulation by oxytocin, indicating that the activated pathway is not linked to the rate of turnover of the Na+ pump.

Animals↗
PubMed1988

Effects of oxytocin on cation content and electrophysiology of frog skin epithelium.

We measured effects of oxytocin on current-voltage (I-V) relations of frog (Rana catesbeiana) skins impaled with an intracellular microelectrode. In both Cl- and Cl(-)-free (SO4(2-) solutions, oxytocin caused an approximate doubling short-circuit current (Isc) and a depolarization of the cell membrane. Increase in apical membrane slope conductance, chord conductance, and permeability after oxytocin correlated with the increase in amiloride-sensitive Isc. Oxytocin also increased basolateral membrane conductance (gb). In Cl-, the shift in the voltage intercept of the apical membrane I-V relation (Ea) implied increased intracellular Na+ activity (a(Na)c) after oxytocin. In isolated frog skin epithelia, a similar increase in intracellular [Na+] after oxytocin was demonstrated by flame photometry. In SO4(2-), changes caused by oxytocin in both Ea and in flame photometrically determined cell [Na+] were minimal. The voltage intercept of the basolateral membrane I-V relations (Eb) was shifted by oxytocin in both Cl- and SO4(2-) solutions. Assuming that the basolateral membrane is selectively permeable to K+, changes in K+ obtained from Eb were in disagreement with those obtained by flame photometry. These results suggest that 1) the increase in a(Na)c caused by oxytocin is not essential to produce either the increase in gb or Isc and 2) ions other than K+ make an important contribution to basolateral membrane conductance.

Animals↗
PubMed1987

Oxytocin and cAMP stimulate monovalent cation movements through a Ca2+-sensitive, amiloride-insensitive channel in the apical membrane of toad urinary bladder.

The effects of oxytocin and cAMP on ion transport were investigated in toad urinary bladders incubated with Ca2+-free solutions on the apical side. Under these conditions both oxytocin and cAMP markedly stimulated the movements of Na+, K+, Rb+, Cs+, Li+, and NH4+ through a pathway that is insensitive to amiloride. The amiloride-insensitive currents were inhibited by the addition of Ca2+, Sr2+, or Mg2+ to the apical solution. The movement of the monovalent cations was associated with a spontaneous Lorentzian component in the power spectrum of the fluctuation in short-circuit current. The plateau of the Lorentzian component was enhanced by oxytocin and cAMP and was depressed by divalent cations. Methohexital inhibited the stimulation of monovalent cation movements caused by oxytocin. These findings suggest that oxytocin and cAMP activate at least two kinds of ionic channels in the apical membrane of toad urinary bladder: the well-known amiloride-sensitive channel and an amiloride-insensitive channel that allows the movement of several monovalent cations and is blocked by Ca2+ and other divalent cations.

Amiloride↗
PubMed1987

Insulin action on electrophysiological properties of apical and basolateral membranes of frog skin.

We measured the effects of insulin on the current-voltage (I-V) relations of frog skins impaled with an intracellular microelectrode. The current across the cell membranes was assumed to be equal to the amiloride-inhibitable current. Insulin increased short-circuit current (Isc) approximately 40% from the control value. The increase in Isc was associated with a depolarization of the cell membrane. In addition there was an increase in the value of the parameters that describe the ease of movement of Na+ across the apical membrane, namely, slope conductance (ga), chord conductance (Ga), and permeability (PNa). The values of these parameters show remarkable linear correlations with membrane current both before and after stimulation. Intracellular Na+ activity (acNa) was determined from the I-V relations of the apical membrane. Insulin did not significantly modify acNa. Insulin also increased the value of the basolateral membrane conductance, however, the relationship between this parameter and current was complex. These experiments show that the stimulatory effect of insulin on Isc is associated with an increase in the conductance of both the apical and basolateral membranes.

Amiloride↗
PubMed1986

K+ -stimulated Na+ transport in frog-skin epithelia.

Increasing [K+] from 2.5 mmol/l to 115 mmol/l on the serosal side of the frog skin produces a rapid decrease of short-circuit current (Isc) that is followed, within a few minutes, by a recovery of Isc to near or above its control value. After isolation of the epithelium by a procedure involving collagenase treatment and physical removal of the corium, increasing serosal [K+] still produced a depression of Isc but no significant recovery phase. By itself, collagenase treatment reduced but did not eliminate the recovery phase. The recovery phase was also markedly depressed by the beta-adrenergic blocker oxprenolol, but not by propranolol, atropine or indomethacin. Amiloride, given during the recovery phase, caused Isc to reverse to a small outward value. These results suggest that the recovery phase of Isc seen in the response to increased serosal [K+] represents an increase in Na+ influx through amiloride-sensitive channels which is triggered by the release of an intermediary agent, possibly a beta-adrenergic agonist, from some structure in the corium.

Adrenergic beta-Antagonists↗
PubMed1986

Oxytocin stimulates the apical K+ conductance in frog skin.

We measured the effects of oxytocin (0.1 U/ml) on the current (Isc) recorded through skins of Rana temporaria incubated with an isotonic K+ solution on the apical side while the transepithelial potential was clamped to zero. Under these conditions, Isc is carried by inward K+ movements. Oxytocin markedly stimulated this inward K+ current. When the spontaneous fluctuations were analyzed we found that oxytocin increased the plateau (S(1)o) of the spontaneous Lorentzian component without modifying the corner frequency (f(1)c). Addition of Ba2+ to the mucosal solution blocked Isc both in the presence and absence of oxytocin. Moreover, with mucosal Ba2+ a characteristic blocker-induced Lorentzian component appeared in the power spectrum. Analysis of this blocker-induced noise showed that oxytocin increased the number of active K+ channels in the apical membrane, while the changes in single channel current were in agreement with the expected alterations of the electrochemical driving force.

Animals↗
PubMed1986

Role of prostaglandin release in the response of tight epithelia to Ca2+ ionophores.

We have studied the effects of the Ca2+ ionophores A23187 and ionomycin on ion transport across amphibian skin and urinary bladder. Both A23187 and ionomycin stimulated transepithelial Na+ transport across the skin. Ionomycin also markedly increased the conductance of an amiloride-insensitive pathway. Both ionophores markedly stimulated the release of prostaglandin E2 (PGE2) into the solution bathing the serosal surface of the skin. Addition of indomethacin to the serosal bathing solution of the skin blocked both the stimulation of short-circuit current (Isc) and the release of prostaglandin caused by the ionophores. Acetylsalicylic acid also blocked the ionomycin-induced stimulation of Isc. These results suggest that the stimulation of Na+ transport caused by Ca2+ ionophores is mediated by the release of a product of the cyclooxygenase pathway, very likely PGE2. Ca2+ ionophores also stimulated the release of PGE2 in urinary bladders; however, they generally depressed Isc. Since the effect on Isc caused by the addition of exogenous PGE2 was different in urinary bladders than in skins, we suggest that at least part of the difference in the action of ionophores is due to the difference in the sensitivity of these epithelia to PGE2. Our results suggest that the heterogeneity of effects that Ca2+ ionophores cause in the physiological parameters of tight epithelia are not always the direct result of increased cytoplasmic Ca2+ but that they may be mediated by other tissue responses triggered by the addition of the ionophores.

Animals↗
PubMed1986

Control of rectal gland secretion in the dogfish (Squalus acanthias): steps in the sequence of activation.

We measured the venous and arterial pressure, as well as the rate of secretion and content of cyclic AMP and high energy phosphate compounds, of the rectal gland of the anaesthetized dogfish, Squalus acanthias (L.). Intravenous infusion of isotonic solutions produced a very large increase in the rate of secretion by the rectal gland. The increase in secretion was preceded by an increase in venous blood pressure, but arterial blood pressure was not modified. Injections of small doses of veratridine stimulated gland secretion when given in the vicinity of the heart but not when given in the dorsal aorta. During volume expansion the creatine phosphate and ATP content of the gland were markedly reduced, while ADP and AMP as well as cyclic AMP content were increased. We conclude that: volume expansion leads to the release of a message that activates adenyl cyclase in the gland; the increased venous pressure may be the initial signal in the sequence that leads to the release of the activating messenger; there is a receptor mechanism in the atrial and cardiac region that triggers the sequence that activates glandular secretion; the reduction in the content of high energy phosphate compounds during volume expansion is caused by an increase in energy expenditure, probably due to gland secretion.

Adenine Nucleotides↗
PubMed1985

Basolateral membrane responses to transport modifiers in the frog skin epithelium.

Application of transepithelial square voltage pulses to the frog skin leads to responses in the transepithelial current and intracellular potential which include transient components. Determinations at 600 ms allow for meaningful estimates of basolateral membrane responses to transport modifiers. Oxytocin produced a large and sustained increase in the amiloride-inhibitable short circuit current (Im) which was accompanied by a large increase of both apical and basolateral membrane conductance (ga and gb, respectively). While Im and ga increased nearly simultaneously, gb started to increase several minutes after the increase in the two other parameters. Insulin also increased Im, ga and gb. As with oxytocin, the increases in Im and ga often preceded the changes in gb. Ouabain reduced Im and ga. The effects on gb were more complex, since sometimes the inhibition of Im was first accompanied by an increase followed by a decrease while in other instances only minor changes in conductance could be observed. The currently available information regarding the control of cytoplasmic [Ca2+] and the effects of Ca2+ on cell membrane properties are used to construct a model in which changes in cytoplasmic [Ca2+] account for the observed behavior of the basolateral membrane.

Animals↗
PubMed1985

Current-voltage relations of the apical and basolateral membranes of the frog skin.

We determined the current-voltage (I-V) relations of the apical and basolateral barriers of frog skins by impaling the cells with an intracellular microelectrode and assuming that the current across the cellular pathway was equal to the amiloride-inhibitable current. We found that: (a) The responses in transepithelial current and intracellular potential to square pulses of transepithelial potential (VT) varied markedly with time. (b) As a consequence of these transient responses, the basolateral I-V relation was markedly dependent on the time of sampling after the beginning of each pulse. The apical I-V plot was much less sensitive to the time of sampling within the pulse. (c) The I-V data for the apical barrier approximated the I-V relations calculated from the Goldman constant field equation over a relatively wide range of membrane potentials (+/- 100 mV). (d) A sudden reduction in apical bath [Na+] resulted in an increase in apical permeability and a shift in the apical barrier zero-current potential (Ea) toward less positive values. The shift in Ea was equivalent to a change of 45 mV for a 10-fold change in apical [Na+]. (e) The transient responses of the skin to square VT pulses were described by the sum of two exponentials with time constants of 114 and 1,563 ms, which are compatible with the time constants that would be produced by an RC circuit with capacitances of 65 and 1,718 microF. The larger capacitance is too large to identify it comfortably with a true dielectric membrane capacitance.

Amiloride↗
PubMed1985

Prostaglandin release mediates drug-induced stimulation of sodium transport in frog skin: the effects of quinacrine.

Quinacrine markedly increased the release of prostaglandin E2 (PGE2) into the basolateral solution of the bullfrog skin from a control value of 32.7 +/- 21.7 pg per 20 min period to a stimulated value of 8593.1 +/- 4112.3 pg per 20 min period. Quinacrine increased the amiloride-sensitive short circuit current from 20.7 +/- 2.1 microA cm-2 to 45.4 +/- 6.5 microA cm-2. The stimulatory effects of quinacrine on both short circuit current and prostaglandin release were blocked in skins pretreated with indomethacin (10(-6) M). Quinacrine did not block either the stimulation of the short circuit current or the increase in PGE2 release caused by the calcium ionophore, ionomycin. These results suggest: (a) the release of PGE2 and the stimulation of the short circuit current caused by quinacrine are linked since blocking PGE2 release inhibits the stimulation of the short circuit current; (b) given the complexity of its actions, quinacrine is a poor tool to examine whether the effects of a given agent are mediated through the activation of endogenous phospholipases. In addition our results taken together with other findings in the literature suggest that there is a diverse group of compounds that stimulate transepithelial sodium transport by releasing PGE2.

Amiloride↗
PubMed1984

Vanadate stimulates the pumped movements of Na in skeletal muscle.

We have measured the effects of concentrations of vanadate ranging between 0.01 and 10 mM on the 22Na efflux of frog sartorius muscles. The addition of vanadate had no effects when concentrations lower than 0.5 mM were used; higher concentrations increased Na efflux. The increase was abolished by the addition of ouabain (10(-5)M). In muscles pretreated with ouabain vanadate did not modify Na efflux. The stimulatory effects of vanadate on Na efflux were also observed in Na-free solutions indicating that the efflux of vanadate was not caused mainly either by an increase in the exchange of Na for Na or by an increase in Na entry into the muscle. We also examined the effects of vanadate on muscles immersed in solutions containing 20 mM K+; both vanadate and increased K+ produced stimulations of Na efflux that were additive. Similarly when the effects of vanadate and insulin were measured on the Na efflux of the same muscle, additive effects were found. As the ouabain-sensitive Na efflux in frog muscle is generally agreed to be due to the activity of the Na-K ATPase, our findings suggest that the net effect of vanadate in intact muscle cells is an increase in the activity of the Na pump. Since vanadate affects many enzymes it is quite possible that the stimulatory action is not due to a direct effect on the Na-K ATPase but may be mediated through an intermediary step.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Noise analysis of inward and outward Na+ currents across the apical border of ouabain-treated frog skin.

The passive Na+ transport across the apical membrane of frog skin (Rana catesbeiana) was studied under the following circumstances: (1) control conditions (sulfate Ringer's, K+ depolarised serosal membranes); (2) after blocking the active transport step with ouabain; (3) with an outward oriented Na+ current. The amiloride-induced Na+ current fluctuations were analysed to calculate the density of amiloride blockable channels and the current through one single channel. Despite the large reduction of the macroscopic current by ouabain, the single channel current remained unchanged, while the number of amiloride blockable Na+ channels was reduced by a factor of eight. It is concluded from these observations that the earlier described reduction of the permeability of the apical membrane is caused by a decrease of the number of electrically conductive Na+ channels. The outward oriented single channel currents were less than 50% of the currents in the opposite direction. After ouabain, the number of Na+ channels was independent from the current direction.

Amiloride↗
PubMed1983

K+-stimulated sugar uptake in skeletal muscle: role of cytoplasmic Ca2+.

We have compared the effects of insulin with those of elevated external K+ concentration ([K+]o) on sugar uptake and protein synthesis by frog skeletal muscle. When [K+]o was between 0.5 and 15 mM there were no effects on uptake; however, when 20 mM was used a significant increase was observed. Further increases in [K+]o caused larger stimulations of uptake. The stimulation persisted for 2.5 h after washing the high [K+]o. The stimulations caused by both insulin and high K+ were markedly inhibited by cytochalasin B. Dantrolene nearly abolished the response to high K+, whereas it had only minor effects on the resting sugar uptake and on the stimulations caused by either insulin or epinephrine. These results suggest that while both insulin and high K+ activate the cytochalasin-sensitive transport system of sugar transport, each agent must act through a different pathway, because only the effects of high K+ were dantrolene sensitive. The effect of dantrolene suggests that the enhancement of sugar transport caused by high K+ is due to an increase of cytoplasmic Ca2+. In contrast to insulin, high K+ did not modify the rate of protein synthesis.

3-O-Methylglucose↗
PubMed1982

Effects of dantrolene and D2O on K+-stimulated respiration of skeletal muscle.

We have examined the effects of dantrolene and D2O on the K+-stimulated respiration in frog skeletal muscle. The threshold for K+ stimulation was around 10 mM extracellular potassium concentration ([K+]o). A further marked increase in respiration to levels about ten times the resting level was noted when [K+]o was between 15 and 20 mM. The increase was sustained for hours when [K+]o was less than 20 mM; however, with higher concentrations the stimulation consisted of an initial burst followed by a decline. Dantrolene shifted the relationship between [K+]o and peak increase in respiration toward higher [K+]o by about 10 mM; in addition it nearly completely blocked the sustained component of the increase. D2O, nearly abolished the K+-induced respiration. Neither agent shifted the relationship between [K+]o and membrane potential nor abolished the stimulation of respiration caused by caffeine. Dantrolene did not block the stimulation of Na+ efflux caused by 15 mM K+. The results with these agents are consistent with the proposal that K+-stimulated respiration is due to Ca2+ release into the cytoplasm. In addition, they provide evidence that the stimulated rate of Ca2+ release into the cytoplasm can remain at a persistently high level for hours provided [K+]o does not exceed 20 mM. We calculated that the level of this constant Ca2+ release is about 3.4 X 10(16) ions/(s.cm3).

Animals↗