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Potassium channel blockers exhibit reverse use-dependent prolongation of the action potential duration. Reverse use dependence is the effect where the efficacy of the drug is reduced after repeated use of the tissue. [11] This contrasts with (ordinary) use dependence, where the efficacy of the drug is increased after repeated use of the tissue.
Example of voltage-dependent potassium ion channel in relation to changing ion concentrations . To comprehend the mechanism of channel blockers, it is critical to understand the composition of ion channels. Their main function is to contribute to the resting membrane potential of a cell via the flow of ions through a cell membrane.
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.
Ion channels are typically categorised by gating mechanism and by the ion they conduct. Note that an ion channel may overlap between different categories. Some channels conduct multiple ion currents and some are gated by multiple mechanisms. Examples of targets for modulators include: Voltage-gated ion channels
The mechanism of potassium channel selectivity remains under continued debate. The carbonyl oxygens are strongly electro-negative and cation-attractive. The filter can accommodate potassium ions at 4 sites usually labelled S1 to S4 starting at the extracellular side.
A potassium channel opener is a type of drug which facilitates ion transmission through potassium channels. Examples. Some examples include:
The mechanism by which minoxidil promotes hair growth is not fully understood. Minoxidil is an adenosine 5'-triphosphate-sensitive potassium channel opener, [25] causing hyperpolarization of cell membranes. Theoretically, by widening blood vessels and opening potassium channels, it allows more oxygen, blood, and nutrients to the follicles.
Quinidine is an inhibitor of the cytochrome P450 enzyme 2D6, and can lead to increased blood levels of lidocaine, beta blockers, opioids, and some antidepressants. Quinidine also inhibits the transport protein P-glycoprotein and so can cause some peripherally acting drugs such as loperamide to have central nervous system side effects, such as ...