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Ionic Basis for Action Potential Prolongation by Phenylephrine in Canine Epicardial Myocytes
Author(s) -
ROBINSON RICHARD B.,
LIU QINYUE,
ROSEN MICHAEL R.
Publication year - 2000
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2000.tb00739.x
Subject(s) - phenylephrine , repolarization , myocyte , purkinje fibers , medicine , endocrinology , ventricle , atrial action potential , electrophysiology , cardiology , blood pressure
Phenylephrine Action on Repolarization. Introduction : In canine ventricle, α‐adrenergic agonists prolong action potential duration (APD) without any effect on the action potential notch, suggesting that, in this species, the effect on repolarization might he independent of inhibition of I to . The present study investigated the action of the α‐adrenergic agonist phenylephrine on the action potential and the repolarizing currents I to and I K in isolated canine epicardial myocytes. Methods and Results : Isolated cells from canine epicardial tissue, and Purkinje fibers, were studied with the whole cell, voltage clamp method. Phenylephrine 0.1 μM increased APD by 13%± 4% at 90% repolarization without affecting the notch or amplitude. Under voltage clamp, concentrations of phenylephrine as high as 10 μM had no effect on I tp in canine epicardial myocytes. However, I to of isolated canine Purkinje myocytes was reduced to 69%± 7% of control by 1 μM phenylephrine. Further studies in canine epicardial myocytes revealed an action of phenylephrine to inhibit I k , and in particular I Ks Using a voltage protocol that included a two‐step repolarization to separate I Ks and I Kr tail components, the largely 1 Ke , component was not significantly affected by 1 μM phenylephrine, whereas the largely I Ks component was reduced to 81%± 5% of control value. Conclusion : α‐Adrenergic prolongation of repolarization in canine epicardium does not result from inhibition of I to . Rather, it appears that reduction of I Ks contributes to the action of phenylephrine. The unresponsiveness of epicardial I to is not a general characteristic of the canine heart, because Purkinje myocyte I to was inhibited, suggesting regional differences in the molecular basis of l to , and/or a‐adrenergic signaling in the canine heart.