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ATP-sensitive potassium channels and cardiac protection (part 10)

ATP-sensitive potassium channels and cardiac protection (part 10)

Whole cell patch clamp recordings revealed time independence and a slight voltage dependence of KATP current in the sense of inward going rectification. The limited outward passage of K+ has been explained by a voltage-dependent block induced by intracellular Mg2+ and Na+ .

It is now clear beyond any doubt that the unambiguous earlier onset of repolarization, loss of plateau and, hence, abbreviation of action potential upon ischemia are due to activation of KATP channels. There are two immediate consequences of the current.First, the calcium influx is cut short and the intracellular Ca2+ available for activation of contraction – the main energy consuming process – is curtailed. The second consequence of increased Katp current is a massive loss of cellular K+. In hypoxia, K+ is permanently removed from the extracellular space and the repolarizing effect of K+ outflow is manifested as hyperpolarization of the resting membrane (in addition to the abbreviation of action potential). Upon ischemia, on the other hand, K+ leaving the cell accumulates in the extracellular space and depolarizes the membranes. Excitability decreases in both instances. The hyperpolarized membrane needs larger local currents to generate action potential, whereas in the depolarized membrane the ability to generate propagated action potentials is mostly lost. Best quality drugs available at best online pharmacy at prices that you are going to enjoy every time: get your cheap asthma inhalers with no problems and no prescription of any kind any time you need some treatment that works 100%.


Category: Cardiology

Tags: ATP-sensitive potassium channel, Ischemic preconditioning, Potassium channel inhibitors, Potassium channel openers

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