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Alpha 1 ‐Adrenergic Receptor Modulation of Repolarization in Canine Purkinje Fibers
Author(s) -
LEE JAE,
ROSEN MICHAEL R.
Publication year - 1994
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.1540-8167.1994.tb01160.x
Subject(s) - purkinje fibers , phenylephrine , repolarization , medicine , agonist , endocrinology , cardiac transient outward potassium current , stimulation , afterdepolarization , adrenergic receptor , electrophysiology , receptor , patch clamp , blood pressure
Alpha‐Agonists and Repolarization. Introduction: Alpha‐adrenergic receptor stimulation increases contractility and prolongs repolarization. These effects are modulated by α 1 ‐adrenergic receptor‐mediated inhibition of transsarcolemmal potassium currents. Methods and Results: We used standard microelectrode techniques to study the actions of 4‐aminopyridine (4‐AP), which blocks the transient outward current, I to , and WAY‐123,398, which blocks the delayed rectifier, I k , on canine Purkinje fiber action potential prolongation induced by phenylephrine. At a basic cycle length of 1 second, phenylephrine (0.1 to 10 μ) dose‐dependently prolonged action potential duration at 90% repolarization (APD 90 ) from 331 ± 10 msec to 400 ± 12 msec (P < 0.05) at phenylephrine, 10 μ. Phenylephrine did not change phase 1 or plateau height. 4‐AP (0.1 mM) decreased phase 1 magnitude, shifted plateau height to more positive potentials (from 0.1 ± 1.8 mV to 14.3 ± 1.1 mV [P < 0.05]), and shortened APD 90 from 318 ± 9 msec to 294 ± 8 msec (P < 0.05). 4‐AP did not block phenylephrine effects on APD 90 , which increased, at 10 μ phenylephrine, from 294 ± 8 msec to 342 ± 6 msec (P < 0.05). In contrast, WAY‐123,398 (0.1 μ) prolonged APD 90 from 360 ± 6 msec to 452 ± 6 msec (P < 0.05), and had no effect on plateau height. In the presence of WAY‐123,398, phenylephrine no longer increased APD 9o . Conclusion: (1) Agents that block I to shorten APD in Purkinje fibers; and (2) the α‐agonist mediated increase of APD in canine Purkinje fibers can be explained by inhibition of I k .