AJP - Heart and Circulatory Physiology, Vol 261, Issue 6 1937-H1944, Copyright © 1991 by American Physiological Society
A model of beta-adrenergic effects on calcium and potassium current in bullfrog atrial myocytes
J. M. Shumaker, J. W. Clark and W. R. Giles
Department of Electrical and Computer Engineering, Rice University, Houston, Texas 7725-1892.
A model of beta-adrenergic and muscarinic cholinergic effects on the
bullfrog atrial myocyte has been developed to simulate the dose-dependent
effects of isoprenaline (Iso) on the action potential duration (APD); i.e.,
low doses of Iso lengthen the APD, whereas high doses shorten the APD. In
this model, the reduction in APD is the result of 1) calcium-dependent
inactivation of calcium current (ICa) resulting from the enhancement of ICa
by Iso and 2) an enhancement of potassium current (IK) due to both an
Iso-induced increase in the rate of activation of IK and an increase in
peak action potential height. The effect of acetylcholine (ACh) is
simulated by a reduction in the Iso-induced increase in ICa and IK through
a reduction in relative adenosine 3',5'-cyclic monophosphate concentration
([cAMP]), as well as activation of the ACh-sensitive potassium current. At
low [Iso] levels in the presence of a high [ACh], the muscarinic
cholinergic effects dominate the beta-adrenergic change. However, for a
large [Iso] and a small [ACh], this pattern of changes in transmembrane
currents is different; in this case the model predicts that ACh can
actually increase APD.
