This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Martynyuk, A. E. Articles by Dennis, D. M. Search for Related Content PubMed PubMed Citation Articles by Martynyuk, A. E. Articles by Dennis, D. M. Related Collections Biochemistry and metabolism Cardiovascular Pharmacology Arrythmias-basic studies

(Circulation. 1999;99:312-318.)
© 1999 American Heart Association, Inc.

Basic Science Reports

Hyperkalemia Enhances the Effect of Adenosine on I_K,ADO in Rabbit Isolated AV Nodal Myocytes and on AV Nodal Conduction in Guinea Pig Isolated Heart

Anatoly E. Martynyuk, PhD, DSc; Timothy E. Morey, MD; Luiz Belardinelli, MD; Donn M. Dennis, MD

From the Departments of Anesthesiology (A.E.M., T.E.M., D.M.D.), Medicine (L.B.), and Pharmacology (L.B., D.M.D.), University of Florida, Gainesville.

Correspondence to Donn M. Dennis, MD, Department of Anesthesiology, University of Florida, PO Box 100254, 1600 SW Archer Rd, Gainesville, FL 32610-0254. E-mail Dennis{at}anest2.anest.ufl.edu

Background—The atrioventricular (AV) node is insensitive to changes in extracellular potassium concentration, [K⁺]_o, because of the absence of the inward rectifier potassium current (I_K1). However, we propose that in the presence of adenosine, elevated [K⁺]_o should increase the adenosine-activated inward rectifier potassium current (I_K,ADO) in AV nodal myocytes and hence augment the negative dromotropic effect of the nucleoside.

Methods and Results—The effects of normal (4.8 mmol/L) and high (8.0 mmol/L) [K⁺]_o on adenosine-induced changes in resting membrane potential (V_m), I_K,ADO, and membrane resistance (R_m) in rabbit isolated AV nodal myocytes and in AV nodal conduction delay (atrium-to-His bundle, AH, interval) in guinea pig isolated hearts were determined with the use of whole-cell patch-clamp and His bundle electrogram techniques, respectively. High [K⁺]_o alone did not significantly affect membrane current, R_m, or V_m in AV nodal myocytes. However, high [K⁺]_o in the presence of adenosine (3 µmol/L) markedly increased I_m (-0.249±0.038 to -0.571±0.111 nA, P<0.05) at -100 mV and reduced R_m (151±21 to 77±8 M, P<0.02). Adenosine still hyperpolarized V_m from -48±2 to -65±1 mV (P<0.001). High [K⁺]_o alone did not significantly affect the AH interval in isolated hearts. However, high [K⁺]_o markedly lengthened the AH interval prolongation caused by adenosine (4 µmol/L, 7.9±0.8 vs 22.1±3.0 ms, P<0.001). The potentiating effect of high [K⁺]_o on adenosine-induced delay in AV nodal conduction was abolished by BaCl₂ (100 µmol/L).

Conclusions—By increasing I_K,ADO and decreasing R_m of AV nodal myocytes, elevated [K⁺]_o, augments the depressant effect of adenosine on AV nodal conduction.

Key Words: adenosine • atrioventricular node • potassium • myocytes

This article has been cited by other articles:

				A. Miyata, J. D. Dowell, D. P. Zipes, and M. Rubart Rate-dependent [K+]o accumulation in canine right atria in vivo: electrophysiological consequences Am J Physiol Heart Circ Physiol, August 1, 2002; 283(2): H506 - H517. [Abstract] [Full Text] [PDF]