A novel action of isoproterenol to inactivate a cardiac K+ current is not blocked by beta and alpha adrenergic blockers

Biophys J. 1990 Sep;58(3):791-5. doi: 10.1016/S0006-3495(90)82422-X.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Biological Transport, Active / drug effects
  • Dogs
  • Drug Interactions
  • Electric Stimulation
  • Electrophysiology
  • In Vitro Techniques
  • Isoproterenol / pharmacology*
  • Potassium / metabolism*
  • Prazosin / pharmacology*
  • Propranolol / pharmacology*
  • Purkinje Fibers / cytology
  • Purkinje Fibers / drug effects*
  • Purkinje Fibers / physiology
  • Yohimbine / pharmacology*

Substances

  • Yohimbine
  • Propranolol
  • Isoproterenol
  • Potassium
  • Prazosin