Effect of local anesthetics on chloride transport in erythrocytes

Rb, Gunn; Ja, Cooper

doi:10.1007/bf01868581

Cited by 29 publications

(4 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Local anesthetics may be primarily Na 1 -channel blockers [17,18], but lidocaine has several beneficial effects that cannot be explained by Na 1channel blocking. It affects properties of the erythrocyte membrane such as cell shape [19][20][21] and chloride transport [22]. Interestingly, several lines of evidence support the conclusion that the G protein-coupled receptor signaling pathway may also be important; the effects of lidocaine on Gia and Gqa functions have been shown to be intensified [23][24][25][26][27][28][29][30][31].…”

Section: Discussionmentioning

confidence: 99%

Functional evidence for presence of lipid rafts in erythrocyte membranes: Gsα in rafts is essential for signal transduction

et al. 2008

View full text Add to dashboard Cite

Membrane microdomains enriched in cholesterol and sphingolipids and containing specific membrane proteins are designated as lipid rafts. Lipid rafts have been implicated in cell signaling pathways in various cell types. Heterotrimeric guanine nucleotide-binding protein (Gsa) has been shown to be a raft component of erythrocytes and has been implicated in cell signaling. Rafts are isolated as detergent-resistant microdomains (DRMs) for biochemical analysis. Cholesterol depletion is widely used to disrupt raft structures to study their function in biological membranes. In the present study, we developed an alternate strategy for disrupting raft structures without altering membrane cholesterol content. Lidocaine hydrochloride, an amphipathic local anesthetic, is shown to reversibly disrupt rafts in erythrocyte membranes and alter the Gsa dependent signal transduction pathway. These findings provide evidence for the presence of rafts while maintaining normal cholesterol content in erythrocyte membranes and confirm a role for raft-associated Gsa in signal transduction in erythrocytes. Am. J. Hematol. 83:371-375, 2008. V

show abstract

Section: Discussionmentioning

confidence: 99%

Functional evidence for presence of lipid rafts in erythrocyte membranes: Gsα in rafts is essential for signal transduction

et al. 2008

View full text Add to dashboard Cite

show abstract

“…Both metabolic rate (Solandt, 1936;Van der Kloot, 1967) and 3-0-methylglucose uptake (Valant & Erlij, 1983) 7-8 7-7 7-6 7-5 7-4 7-3 7*2 pHi 7-1 7-0 6-9 6-8 6-7 (Hille, 1977); Ca release induced by either depolarization or caffeine in frog skeletal muscle (Luttgau & Oetliker, 1968;Almers & Best, 1976); K permeability in frog muscle (Liuttgau & Oetliker, 1968); and pHi recovery in frog muscle (Abercrombie & Roos, 1981 (Gunn & Cooper, 1975). This exchange differs from that in frog muscle by lacking a requirement for Na.…”

Section: Resultsmentioning

confidence: 99%

Effect of calcium and other divalent cations on intracellular pH regulation of frog skeletal muscle.

Putnam¹,

Roos²

1986

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. We examined, in frog semitendinosus muscle, the effect of calcium release, induced by depolarization or caffeine, on intracellular pH (pHi) recovery from an acid load applied at least 40 min later. We also studied the effect of external Ca and other divalent cations on recovery. We used pH-sensitive micro-electrodes; the external pH (pHO) was always 7.35.2. In fibres depolarized by 50 mM-K, constant [K] x [Cl] in the presence of 1 mM-tetracaine (which blocks Ca release), the rate of pHi recovery from 5 % C02-induced acidification was 0415+0-02 ApHi h-1 (n = 7), whereas in depolarized fibres that had never been exposed to the drug, the rate of recovery was 0'27 + 0-01 ApH1 h-1 (n = 5). Yet, when Ca release was not blocked and the depolarized fibres were exposed to tetracaine shortly before CO2 exposure, a similar slow rate of 0-14+0-03 ApHi h-1 (n = 7) was observed. When Ca release was blocked by tetracaine, but the drug washed out before recovery, the rate was again 0-27 + 002ApHi h-1 (n = 6).3. In fibres first depolarized to about -23 mV in 50 mM-K, constant [K] x [Cl] (recovery of023 + 0 03 ApHi h-1, n = 6), and then repolarized to -79 mV in 2-5 mM-K, the slow rate of recovery was the same (0 03 + 0-02 ApHi h-') as that in fibres without a history of depolarization and thus of Ca release.4. In fibres depolarized to -50 mV (15 mM-K, constant Cl) and then exposed to caffeine (4 mM) which releases Ca from intracellular stores, the recovery was the same (0-07 + 0-03 ApHi h-1, n = 5) as in depolarized fibres not exposed to caffeine (0-09+0-01 ApHi h-1, n = 5).5. We conclude that in frog muscle transient Ca release induced by either depolarization or caffeine does not affect the rate of subsequent pHi recovery. Tetracaine reversibly inhibits pHi recovery, but this inhibition is not due to its blocking of Ca release.6. Recovery from C02-induced acidification of fibres depolarized to -21 mV in 50 mM-K, constant Cl was halved, from 0-31 +0-04 ApHi h-1 (n = 10) to 0-15+0-01ApHi h-1 (n = 13), when external Ca was raised from 4 to 10 mm. There was no further reduction in recovery at 14 mM-Ca (0 15+0-04 ApHi h-1, n = 4). Lowering Ca 7. Ba at 4, 10 or 20 mm reduced recovery from CO2 acidification to 0-19 + 001 (n = 5), 0 16 + 0-01 (n = 6) and 0 13 + 0-03 ApHi h-1 (n = 5), respectively. Mg at 8 mM or Sr at 6 mm had no effect on recovery, but 20 mM-Mg or Sr reduced recovery to 0-23 + 002 ApHi h-' (n = 6), respectively. Ni or Cd, each at 1 mm, reduced recovery to 0-21 + 001 ApHi h-1 (n = 6) and 0-12 + 0-02 ApHi h-1 (n = 7), respectively. 8. The reduced recovery from CO2-induced acidification in 10 mM-Ca was not affected by 1 mM-amiloride (015 +0-01 ApHi h-1, n = 8), even though we previously found that amiloride reduced the higher recovery rate observed in 4 mM-Ca by about 50 %. 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS) (0 1 mm) nearly abolished the recovery in 10 mM-Ca (0-05 + 002 ApHi h-1, n = 11). We conclude that elevated external Ca preferentially inhibits Na-H exchange.9. In agreeme...

show abstract

“…Using Eq. (27) for the estimation of k~0 and assuming a number of 1 x 106 anion adsorption sites per cell, we end up with a translocation rate of 31 sec-1 at 37 ~ and of 8 sec -1 at 25 ~ for sulfate. Brahm [4] (Table 2) reveals that the dielectric constant of the pores should be between 10 and 15.…”

Section: (27)mentioning

confidence: 99%

“…The frequency at which this occurs is determined by the free energy of activation A F~, which is the change in energy necessary for the ith ion to pass from its current equilibrium position in front of the barrier to the top of the energy barrier. The rate constant #~o for a diffusive jump can therefore be written as [16,22,27]:…”

Section: Transport Of Anions Across the Membranementioning

confidence: 99%

Anion transport across the red blood cell membrane mediated by dielectric pores

Schnell

1977

J. Membrain Biol.

View full text Add to dashboard Cite

Summary. The anion transport across the red blood cell membrane is assumed to occur by ionic diffusion through dielectric pores which are formed by protein molecules spanning the red blood cell membrane. The access of anions to the dielectric pores is regulated by anion adsorption sites positioned at the entrances of the pores. The adsorption of small inorganic anions to the adsorption sites is facilitated by ionizing cationic groups setting up a surface potential at the respective membrane surfaces. Applying the transition state theory of rate processes, flux equations for the unidirectional flux were derived expressing the unidirectional flux as a function of the fractional occupancies of anion adsorption sites at both membrane surfaces.The basic properties of the transport model were investigated. The concentrationdependence and the pH-dependence of the unidirectional fluxes were shown to depend upon the surface charge density and upon the affinity of the transported anion species to the anion binding sites. The concentration-response and the pH-response of the unidirectional fluxes of different anion species may differ substantially even if the anion species are transported by the same anion transport system. The model predicts a characteristic behavior of the Lineweaver-Burk plot and of the Dixon plot.A comparison between computer simulated and experimentally determined flux curves was made. By choosing a suitable set of parameters, the anion transport model is capable of simulating the concentration-dependencies and the pH-dependencies of the unidirectional sulfate and chloride flux. It is sufficient to change one single constant in order to convert the "sulfate transport system" into a "chloride transport system". Furthermore, the model is capable of predicting the inhibitory action of chloride on the sulfate transport system. No attempts were made to fit the experimental data to the model. The behavior of the model was qualitatively in accordance with the experimental results.The kinetics of the anion transport across the red blood cell membrane displays a number of features which are indicative of a specific transport system. The anion permeability of the erythrocyte membrane is many orders of magnitude higher than the anion permeability of an

show abstract

Effect of local anesthetics on chloride transport in erythrocytes

Cited by 29 publications

References 21 publications

Functional evidence for presence of lipid rafts in erythrocyte membranes: Gsα in rafts is essential for signal transduction

Functional evidence for presence of lipid rafts in erythrocyte membranes: Gsα in rafts is essential for signal transduction

Effect of calcium and other divalent cations on intracellular pH regulation of frog skeletal muscle.

Anion transport across the red blood cell membrane mediated by dielectric pores

Contact Info

Product

Resources

About