Adrenergic control of the ultrarapid delayed rectifier current in canine atrial myocytes.

摘要

1. The effects of adrenergic stimulation on the ultrarapid delayed rectifier K+ current (IKur,d) of dog atrial myocytes was studied with patch-clamp methods. 2. Isoproterenol (isoprenaline) increased IKur,d in a concentration-dependent fashion with an EC50 of 7.3 +/- 0.8 nM. The effect of isoproterenol was blocked by propranolol, mimicked by forskolin and 8-bromo-cAMP, and prevented by inhibition of protein kinase A. 3. Phenylephrine (in the presence of propranolol) increased IKur,d with an EC50 of 0.49 +/- 0.06 microM. The effect of phenylephrine was blocked by prazosin, prevented by inhibition of protein kinase C, and mimicked by activation of protein kinase C with phorbol ester. 4. Phenylephrine significantly abbreviated canine atrial action potential duration in the absence of tetraethylammonium (TEA). When TEA was present under both control conditions and in the presence of phenylephrine, phenylephrine failed to alter canine atrial repolarization. 5. We conclude that beta- and alpha-adrenergic stimulation increase IKur,d via protein kinase A and C, respectively, and that the induced changes in IKur,d may play a role in adrenergic control of canine atrial repolarization.