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Sodium channel blockers are also used as local anesthetics and anticonvulsants. [5] Sodium channel blockers have been proposed for use in the treatment of cystic fibrosis, [6] but current evidence is mixed. [7] It has been suggested that the analgesic effects of some antidepressants may be mediated in part via sodium channel blockade. [8]
Introducing specific sodium channel blockers into a tissue allows for the preferential binding of the blocker to sodium channels, which results in an ultimate inhibition of the flow of sodium into the tissue. Over time, this mechanism leads to an overall decrease in tissue excitation.
An epithelial sodium channel blocker is a sodium channel blocker that is selective for the epithelial sodium channel. An example is amiloride , which is used in the treatment of hypertension . [ 1 ]
Procainamide (PCA) is a medication of the antiarrhythmic class used for the treatment of cardiac arrhythmias.It is a sodium channel blocker of cardiomyocytes; thus it is classified by the Vaughan Williams classification system as class Ia.
Pharmacological blockers of INaP are used clinically in many of these disorders. Amiodarone, while primarily blocking the human Ether-a-go-go-Related Gene potassium channel, has shown to significantly reduce persistent sodium current by 50% in cortical neurons [14] as well as in cardiac sodium channel NaV1.5 and is used to treat arrhythmia. [15]
Flecainide works by blocking the Nav1.5 sodium channel in the heart, slowing the upstroke of the cardiac action potential. [32] This thereby slows conduction of the electrical impulse within the heart, i.e. it "reduces excitability". The greatest effect is on the His-Purkinje system and ventricular myocardium. The effect of flecainide on the ...
DSP-2230 is a selective small-molecule Na v 1.7 and Na v 1.8 voltage-gated sodium channel blocker which is under development by Dainippon Sumitomo Pharma for the treatment of neuropathic pain. [ 1 ] [ 2 ] As of June 2014, it is in phase I / phase II clinical trials .
Class IV agents are slow non-dihydropyridine calcium channel blockers. They decrease conduction through the AV node , and shorten phase two (the plateau) of the cardiac action potential . They thus reduce the contractility of the heart, so may be inappropriate in heart failure.
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