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Sodium efflux

Pharmacology The primary site of action of hydantoins appears to be the motor cortex, where spread of seizure activity is inhibited. Possibly by promoting sodium efflux from neurons, hydantoins tend to stabilize the threshold against hyperexcitability. [Pg.1209]

Stabilizes the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient, possibly by promoting sodium efflux from neurons... [Pg.141]

Prokaryotic organisms have developed a number of transport mechanisms for the extrusion of sodium ions against a concentration gradient. In Escherichia coli sodium efflux is linked to proton uptake and is independent of internal ATP, i.e. the cell uses a sodium/proton antiporter.70,71 In contrast in Streptococcus faecalis,72 sodium efflux involves an ATP-driven sodium-translocating ATPase, while in Halobacterium halobium the protein halorhodopsin has been postulated to catalyze the coupling of Na+ extrusion to light.73... [Pg.558]

Epilepsy is a neurological disorder characterized by recurrent spontaneous seizures due to an imbalance between cerebral excitability and inhibition, with a tendency towards uncontrolled excitability (Papandreou et al., 2006). Recurrent severe seizures can lead to death of brain cells. Phenytoin (Dilantin, Phenytek) is a widely used anti-seizure medicine (LaRoche, 2007). The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited, possibly by promoting sodium efflux from neurons. Phenytoin tends to stabilize the threshold against hyper-excitability caused by excessive stimulation. The current status of new (second generation) anti-epileptic drugs has been recently reviewed (Bialer et al., 2007). [Pg.262]

Impaired sodium efflux was measured in leukocytes from patients with essential hypertension. Incubation of normal leukocytes with plasma from hypertensive patients caused impaired sodium transport. 6 Furthermore, partially purified fractions from plasma, as well as urine, inhibit sodium efflux from peripheral blood leukocytesThe severity of the defect in leukocyte cation transport is inversely related to the plasma renin activity and is greatest in patients with essential hypertension in whom the renin response to sodium restriction was atypical. Although these studies support the hypothesis that NH is a digitalis-like substance which inhibits Na, K -ATPase in numerous tissues including the kidney, it remains to be determined whether the natriuretic effect of NH is due exclusively to inhibition of renal Na, K -ATPase. [Pg.255]

Sodium fluxes were computed by multiplying the measured flow of radioactivity in cpm/cmYs by the reciprocal of the specific activity of the solution measured in pmol, 10 M/cpm. Fig. 2b shows part of the time course of a typical sodium efflux experiment. Intracellular perfusion was begun with 600 mM KF after 13 min, this solution was replaced by 500 mM KF, 100 mM NaF and then, after 23 min, by a solution of the same composition, but with Na added. [Pg.72]

It is clear from this figure that the sodium influx again remained almost constant during the internal perfusion with a given sodium concentration. Table 1 summarises the data on resting sodium fluxes obtained by internal perfusion with different concentrations of sodium. As shown in Table 1 the resting sodium efflux is affected by the internal sodium concentration. There is an increase in sodium efflux from 0.1 pmol/cm s to 34 pmol/cm s as the internal sodium concentration is increased from 2 to 200 mM. To calculate resting values from the data in Table 1 we... [Pg.72]

Figure 36. Diagram illustrating movements of ions through a nerve cell membrane. The downhill movements which occur during the impulse are shown on the right uphill movements during recovery are shown on the left. The broken line represents the component of the sodium efflux which is not abolished by removing external potassium ions. (From Reference 196). Figure 36. Diagram illustrating movements of ions through a nerve cell membrane. The downhill movements which occur during the impulse are shown on the right uphill movements during recovery are shown on the left. The broken line represents the component of the sodium efflux which is not abolished by removing external potassium ions. (From Reference 196).
Guy SP, Jones D, Mann DMA, Itzhaki RF (1991) Human neuroblastoma cells treated with aluminium express, an epitope associated with Alzheimer s disease neurofibrillary tangles. Neurosci Lett 121 166-168 Hollosi M, Urge L, Perczel A, Kajtar J, Teplan I, Otvos L Jr, Fasman GD (1992) Metal ion-induced conformational changes of phosphorylated fragments of human neurofilament (NF-M) protein. J Mol Biol 223 673-682 Huang Y-P, Bittar EE (1991) Protection by GTP from the effects of aluminum on the sodium efflux in barnacle muscle fibers. Biochim Biophys Acta 1062 255-263 Huber CT, Frieden E (1970) The inhibition of ferroxidase by trivalent and other metal ions. J Biol Chem 245 3979-3984... [Pg.158]

Fio. 2. The effect of ouabain on the sodium efflux from a squid axon. At the first arrow the compound is applied internally using a microsyringe. At the second arrow 10 M ouabain is added to the sea water outside. (After Caldwell, P. C. and... [Pg.194]

Bittar, E.E. Xiang, Z. Huang, Y.P. (1992) Citrate as an aluminium chelator and pwsitive effector of the sodium efflux in single batnade muscle fibers, Biodiim Biofdiys Acta, Vol. 1108, pp. 210-214. [Pg.294]

Borzak, S. Reers, M. Arruda, J. Sbarma, V. K. Sbeu, S. S. Smitb, X. W. Marsb, J. D. Sodium efflux mechanisms in ventricular myocjdes measurement of [Na "]i with sodium-binding benzofuran isophthalate. Am. J. Physiol. 1992,263, H866-H874. [Pg.432]

BAL—see Propan-l-ol, 2,3-dimercapto-Bacillus cereus calcium transport, 6,572 Bacillus megaterium calcium efflux, 6, 570 calcium transport, 6,572 sporulation zinc transport, 6, 572 Bacillus spp. sodium ions, 6, 559 sporulation... [Pg.89]

Juel, C. (1988), Intracellular pH recovery and lactate efflux in mouse soleus muscles stimulated in vitro The involvement of sodium/proton exchange and a lactate carrier. Acta Physiol. Scand. 132,... [Pg.277]

Both influx and efflux transporters are located in intestinal epithelial cells and can either increase or decrease oral absorption. Influx transporters such as human peptide transporter 1 (hPEPTl), apical sodium bile acid transporter (ASBT), and nucleoside transporters actively transport drugs that mimic their native substrates across the epithelial cell, whereas efflux transporters such as P-glycoprotein (P-gp), multidrug resistance-associated protein (MRP), and breast cancer resistance protein (BCRP) actively pump absorbed drugs back into the intestinal lumen. [Pg.500]

Sodium channels open more rapidly than K+ channels because they are more voltage sensitive and a small depolarization is sufficient to open them. Larger changes in membrane potential associated with further cell excitation are required to open the less voltage-sensitive K+ channels. Therefore, the increase in the permeability of K+ ions occurs later than that of Na+ ions. This is functionally significant because if both types of ion channels opened concurrently, the change in membrane potential that would occur due to Na+ ion influx would be cancelled out by K+ ion efflux and the action potential could not be generated. [Pg.27]

Cummins, C. L., Mangravite, L. M., Benet, L. Z., Characterizing the expression of CYP3A4 and efflux transporters (P-gp, MRP1, and MRP2) in CYP3A4-transfected Caco-2 cells after induction with sodium butyrate and the phorbol ester 12-0-tetradecanoylphorbol-13-acetate,... [Pg.187]

For example, the stimulation of )6-adrenoceptors by noradrenaline results in the activation of adenylate cyclase on the irmer side of the nerve membrane. This enz)nne catalyses the breakdown of ATP to the very labile, high-energy compound cyclic 3,5-adenosine monophosphate (cyclic AMP). Cyclic AMP then activates a protein kinase which, by phosphorylating specific membrane proteins, opens an ion charmel to cause an efflux of potassium and an influx of sodium ions. Such receptors are termed metabotropic receptors. [Pg.25]

Mecfianism of Action An antiarrhythmic that decreases sodium influx during depolarization, potassium efflux during repolarization, and reduces calcium transport across the myocardial cell membrane.Decreases myocardial excitability, conduction velocity, and contractility Therapeutic Effect Suppresses arrhythmias. Pharmacokinetics Almost completely absorbed after PO administration. Protein binding 80%-90%. Metabolized in liver. Excreted in urine. Removed by hemodialysis. Half-life 6-8 hr. [Pg.1068]


See other pages where Sodium efflux is mentioned: [Pg.159]    [Pg.258]    [Pg.148]    [Pg.339]    [Pg.287]    [Pg.552]    [Pg.72]    [Pg.73]    [Pg.160]    [Pg.159]    [Pg.258]    [Pg.148]    [Pg.339]    [Pg.287]    [Pg.552]    [Pg.72]    [Pg.73]    [Pg.160]    [Pg.110]    [Pg.109]    [Pg.36]    [Pg.170]    [Pg.173]    [Pg.193]    [Pg.322]    [Pg.346]    [Pg.370]    [Pg.171]    [Pg.421]    [Pg.433]    [Pg.170]    [Pg.223]    [Pg.17]    [Pg.27]    [Pg.31]    [Pg.103]    [Pg.113]   


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