title: Adenosine increases potassium conductance in isolated rabbit atrioventricular nodal myocytes.
abstract: 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 degrees 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 microM) 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(-)N(6)-(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.
authors.affiliation: Department of Medical Cardiology, Royal Infirmary, Glasgow, UK.
authors.forename: A E
authors.initials: AE
authors.lastname: Martynyuk
authors.forename: K A
authors.initials: KA
authors.lastname: Kane
authors.forename: S M
authors.initials: SM
authors.lastname: Cobbe
authors.forename: A C
authors.initials: AC
authors.lastname: Rankin
mesh_terms: D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D001283:Atrioventricular Node / Q000187:drug effects / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000187:drug effects; D002478:Cells, Cultured; D008564:Membrane Potentials / Q000187:drug effects; D018408:Patch-Clamp Techniques; D010660:Phenylisopropyladenosine / Q000494:pharmacology; D058915:Purinergic P1 Receptor Antagonists; D011817:Rabbits; D000254:Sodium-Potassium-Exchanging ATPase / Q000187:drug effects*; D013268:Stimulation, Chemical; D014970:Xanthines / Q000494:pharmacology
chemical_list: D058915:Purinergic P1 Receptor Antagonists; D014970:Xanthines; D010660:Phenylisopropyladenosine; C051360:1,3-dipropyl-8-cyclopentylxanthine; D000252:Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase; D000241:Adenosine