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The delayed rectifier potassium current (IK) is a major outward current responsible for ventricular muscle action potential repolarization.In most species,IK can be separated into rapid (IKr) and slow (IKs) components that differ from one another in terms of their sensitivity to drugs, rectification characteristics,and kinetic properties.IKs is known to be enhanced by elevation of the intracellular cAMP level, therefore the current is augmented during increased sympathetic tone.Adrenergic stimulation results in the release of the adrenergic hormones,catecholamines, including norepinephrine (noradrenaline) from, post-ganglionic nerve terminals, and adrenaline (epinephrine) from the adrenal medulla.Our study wants to illustrate the modulation and underlying signal transduction mechanisms of norepinephrine on the slow component of delayed retifier potassium current.IKs was recorded from guinea-pig atrial myocytes, using the whole-cell configuration of patch-clamp method.Application of norepinephrine 10 M enhanced IKs by 69.54±2.5% concentration-dependently with EC50 of 562.97 nM.The current of IKs induced by adrenaline can be inhibited by 293B of 30 M.To further examine the signal transduction pathways mediating the inhibitory action of norepinephrine on IKs.We will definite which type of PKC isoforms norepinephrine involved in this PKC action.