Skip Navigation

Cardiovascular Research 1995 30(5):668-675; doi:10.1016/S0008-6363(95)00078-X
© 1995 by European Society of Cardiology
This Article
Right arrow Full Text (PDF)
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Martynyuk, A.E.
Right arrow Articles by Rankin, A.C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Martynyuk, A.E.
Right arrow Articles by Rankin, A.C.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1995, European Society of Cardiology

Adenosine increases potassium conductance in isolated rabbit atrioventricular nodal myocytes

A.E. Martynyuka,1, K.A. Kaneb, S.M. Cobbea and A.C. Rankin*

aDepartment of Medical Cardiology, Royal Infirmary, 10 Alexandra Parade, Glasgow G31 2ER, UK
bDepartment of Physiology and Pharmacology, University of Strathclyde, Glasgow, UK

* Corresponding author., Tel.: (+44-141) 552-3535; fax: (+44-141) 552-4683.

Objective: To study the actions of adenosine on the electrophysiology of spontaneously active, rod-shaped cells enzymatically isolated from rabbit atrioventricular (AV) node. Methods: Calcium-tolerant myocytes were isolated from the region of the AV node by enzymatic and mechanical dispersion. They were rod- or spindle-shaped, with spontaneous activity at 35–37 °C, and had higher membrane resistances (776 ± 283 M{Omega}, n = 13), compared to atrial cells (41 ± 18.2 M{Omega}, n = 7; P < 0.001). Membrane potential, spontaneous action potentials and transmembrane ionic currents were studied using the whole-cell patch-clamp technique, in current-clamp and voltage-clamp mode. Results: Adenosine (0.1–50 µM) slowed or abolished the spontaneous activity, with hyperpolarisation of the membrane potential. Voltage-clamp experiments showed that adenosine induced an inwardly rectifying time-independent current. The adenosine-induced current was shown to be carried by potassium ions by the effect of increasing external potassium, which altered the reversal potential in accordance with the calculated potassium equilibrium potential. The A1 adenosine receptor antagonist, CPDPX (8-cyclopentyl-1,3-dypropylxanthine), reversed the effects of adenosine and an A1 receptor agonist, R-PIA [R(–)N6-(2-phenylisopropyl)adenosine] had effects similar to adenosine. Adenosine also caused a small decrease in inward calcium current (ICa) in some AV nodal cells. Conclusions: These results indicate that adenosine acts at A1 adenosine receptors to suppress spontaneous activity, hyperpolarise membrane potential and induce a time-independent potassium current in AV nodal cells. These actions, combined with reduction in inward calcium current in some cells, may underlie the negative chronotropic and dromotropic actions of adenosine on rabbit AV nodal cells.

KEYWORDS Adenosine; Atrioventricular node; A1-receptors; Potassium channel, background; Membrane potential; Rabbit, AV nodal cells


1 Permanent address: A.A. Bogomoletz Institute of Physiology, Bogomoletz Str. 4, 252601 GSP, Kiev 24, Ukraine.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Cardiovasc ResHome page
A. J Workman, K. A Kane, and A. C Rankin
Ionic basis of a differential effect of adenosine on refractoriness in rabbit AV nodal and atrial isolated myocytes
Cardiovasc Res, September 1, 1999; 43(4): 974 - 984.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.