A novel action of isoproterenol to inactivate a cardiac K+ current is not blocked by beta and alpha adrenergic blockers.
The K+ current iKl sets the resting potential in cardiac cells. Here we report that isoproterenol (ISO), a prototypical beta agonist, increases inactivation of iKl. This action of ISO on iKl is mimicked by permeant analogues of cAMP but is not blocked by the beta blockers propranolol and pindolol or the alpha blockers prazosin or yohimbine. We suggest that this novel action of ISO may contribute to pacemaker activity in the Purkinje strand and be mediated through a class of receptors different from classical beta's or alpha's.
Department of Physiology and Biophysics, State University of New York, Stony Brook 11794.
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D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D004285:Dogs; D004347:Drug Interactions; D004558:Electric Stimulation; D004594:Electrophysiology; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism*; D011224:Prazosin / Q000494:pharmacology*; D011433:Propranolol / Q000494:pharmacology*; D011690:Purkinje Fibers / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D015016:Yohimbine / Q000494:pharmacology*
D015016:Yohimbine; D011433:Propranolol; D007545:Isoproterenol; D011188:Potassium; D011224:Prazosin