These studies were supported by USPHS-NHLBI Grants HL-67449 and HL-28958.
Adrenergic-Cholinergic Interaction that Modulates Repolarization in the Atrium is Altered with Aging
Version of Record online: 12 AUG 2003
© Futura Publishing Company, Inc. 2002
Journal of Cardiovascular Electrophysiology
Volume 13, Issue 4, pages 374–379, April 2002
How to Cite
SOSUNOV, E. A., ANYUKHOVSKY, E. P. and ROSEN, M. R. (2002), Adrenergic-Cholinergic Interaction that Modulates Repolarization in the Atrium is Altered with Aging. Journal of Cardiovascular Electrophysiology, 13: 374–379. doi: 10.1046/j.1540-8167.2002.00374.x
- Issue online: 12 AUG 2003
- Version of Record online: 12 AUG 2003
- Manuscript received 20 December 2001; Accepted for publication 25 February 2002.
- Cited By
- atrial action potential;
- accentuated antagonism;
Autonomic Modulation of Atrial Repolarization.Introduction: Aging is associated with involution of both limbs of the autonomic nervous system, and the prejunctional and postjunctional effects of adrenergic and cholinergic stimulation are altered with senescence. Hence, postjunctional age-related changes in adrenergic-cholinergic interaction are a likely occurrence and may contribute to an altered substrate for arrhythmias.
Methods and Results: Microelectrode techniques were used to record action potentials from epicardial slices of Bachmann's bundles of dogs aged 3 to 5 years (adult) and 8 to 12 years (old) in the absence or presence of acetylcholine and isoproterenol (separately and in combination). In control, action potential duration to 90% repolarization (APD) was longer in old atria. Acetylcholine (10−8 to 10−5 mol/L) in a concentration-dependent manner hyperpolarized and shortened APD in both tissues, with more prominent effects in the old. The effects of isoproterenol (10−9 to 10−6 mol/L) to elevate the plateau and shorten APD were about the same in both adult and old tissues. In adults, low concentrations of isoproterenol (10−9 and 10−8 mol/L) significantly prolonged APD, which had been first shortened by acetylcholine. This effect of isoproterenol was decreased in old atrial tissue, resulting in shorter APD in old than adult atria in the combined presence of beta-adrenergic and muscarinic agonists. Conclusion: In adult Bachmann's bundle, beta-adrenergic stimulation effectively operates as a “brake” to decrease the extent of cholinergic-induced APD shortening. The action of beta-adrenergic stimulation to antagonize acetylcholine-induced acceleration of repolarization declines with age, which may contribute to an altered arrhythmogenic substrate.