Catecholamines modulate the delayed rectifying potassium current (IK) in guinea pig ventricular myocytes.
The effects of isoproterenol and norepinephrine on the delayed, outward potassium current, IK, were tested in single, dialyzed guinea pig heart cells where complications from a restricted extracellular space are minimized and internal K concentration is controlled. The average IK reversal potential in control cells was -80 +/- 2.1 mV (N = 4; [K]o = 4.5 mM; [K]i = 120 mM) indicating a high degree of K selectivity (PNa/PK less than or equal to 0.01). In paired experiments, both isoproterenol and norepinephrine increased IK without changing the reversal potential, indicating that the selectivity of the channels is not altered by these agents. The results explain the shortening of action potential duration observed at high concentrations (Quadbeck and Reiter, 1975); and suggest that an increase in IK by catecholamines may serve to limit the degree of calcium current-induced action potential prolongation during increased sympathetic tone and rapid heart rates.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects*; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects*; D007545:Isoproterenol / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism*
D007473:Ion Channels; D007545:Isoproterenol; D011188:Potassium; D009638:Norepinephrine