Exemplos de uso de Sodium channels em Inglês e suas traduções para o Português
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Sodium Channels.
Blockers of sodium channels(Duspatalin);
Kurtoxin also has an effect on sodium channels.
It also blocks sodium channels in the central and peripheral nervous systems.
This is achieved by blocking sodium channels.
Nerve cells called sodium channels and calcium channels. .
Like other TCAs,clomipramine weakly blocks voltage-dependent sodium channels as well.
The toxin blocks sodium channels, blacking out the body's nervous system.
Usually, it blocks opened ion channels, similar to the susceptible state of sodium channels.
Carbamazepine: blocks sodium channels at the presynaptic and postsynaptic levels.
They block serotonin and norepinephrine reuptake,NMDA agonist-induced hyperalgesia and block sodium channels.
Lidocaine affinity for sodium channels is higher in open and inactivated states.
Zonisamide works by blocking specific pores on the surface of nerve cells called sodium channels and calcium channels. .
Voltage-gated sodium channels Nav represent the classical targets of lidocaine.
Mechanism of action Rufinamide modulates the activity of sodium channels, prolonging their inactive state.
Sodium channels are key proteins for action potentials upstroke in excitable cells.
Rufinamide modulates the activity of sodium channels, prolonging their inactive state.
Blockade of sodium channels slows the rate and amplitude of initial rapid depolarization, reduces cell excitability, and reduces conduction velocity.
Furthermore, gabapentin can act on NMDA receptors, sodium channels, monoaminergic pathways, and opioid system.
The opening of sodium channels allows nearby sodium channels to open, allowing the change in permeability to spread from the dendrites to the cell body.
Definition English: A family of proton-gated sodium channels that are primarily expressed in neuronal tissue.
It is known that voltage-dependent sodium channels affinity is higher with dextrogyrous enantiomers R as compared to levogyrous enantiomers S, being the former more toxic to the cardiovascular system.
The blockade is exerted, especially, on tetrodotoxin-sensitive sodium channels TTX-S, which are associated with neuronal lesion.
Bupivacaine could rapidly block sodium channels during action potential, however with slower dissociation as compared to lidocaine.
In vitro electrophysiological studies have shown that lacosamide selectively enhances slow inactivation of voltage-gated sodium channels, resulting in stabilization of hyperexcitable neuronal membranes.
The R isomer shows stronger binding to sodium channels and slower dissociation than the S isomer, which is responsible for its lower cardiotoxicity.
The aim of this study was to evaluate the expression of voltage-gated sodium channels(nav) and their subcellular location in neurons of different formations of na and dmv.
Carbamazepine blocks voltage-gated sodium channels, delays ionic recovery after activation and suppresses spontaneous activity without blocking normal conduction.
The expressiveness of the sodium channels was evaluated in the individuals.
Lamotrigine blocks voltage-gated sodium channels and inhibits glutamate and aspartate release.