Electrophysiologic effects of adenosine triphosphate on rabbit sinoatrial node pacemaker cells via P1 receptors
Abstract
AIM: To study the electrophysiologic effects of adenosine triphosphate (ATP) on rabbit sinoatrial node pacemaker cells and the receptors related with the action of ATP.
METHODS: Intracellular microelectrode method was used to record the parameters of action potential (AP) in the rabbit sinoatrial nodes.
RESULTS: ATP (0.1-3 mmol/L) decreased the rate of pacemaker firing (RPF) by 16 %-43 % and velocity of diastolic depolarization (VDD) by 33 %-67 %, increased the amplitude of AP (APA) by 6 %-9 % and maximal rate of depolarization (V(max)) by 30 %-76 %, shortened APD50 by 7 %-12 % and APD(90) by 6.3 %-9 %, concentration-dependently. The effects of ATP, adenosine (Ado), and adenosine diphosphate at the same concentration on AP were not different from each other significantly. Neither uridine triphosphate nor alpha,beta-methylene ATP had significant electrophysiologic effects on the sinoatrial node of rabbits. Both the electrophysiologic effects of ATP and Ado on pacemaker cells were inhibited by P1 receptor antagonist aminophylline 0.1 mmol/L (P<0.05) in a closely similar manner, and the effects of ATP were not affected by P2 receptor antagonist reactive blue 2 at 0.05 mmol/L (P>0.05).
CONCLUSION: There are no functional P2X(1) and P2Y(2) receptors on pacemaker cells of the rabbit sinoatrial nodes, and the electrophysiologic effects of ATP in the rabbit sinoatrial node pacemaker cells are mediated via P1 receptors by Ado degraded from ATP.
Keywords:
METHODS: Intracellular microelectrode method was used to record the parameters of action potential (AP) in the rabbit sinoatrial nodes.
RESULTS: ATP (0.1-3 mmol/L) decreased the rate of pacemaker firing (RPF) by 16 %-43 % and velocity of diastolic depolarization (VDD) by 33 %-67 %, increased the amplitude of AP (APA) by 6 %-9 % and maximal rate of depolarization (V(max)) by 30 %-76 %, shortened APD50 by 7 %-12 % and APD(90) by 6.3 %-9 %, concentration-dependently. The effects of ATP, adenosine (Ado), and adenosine diphosphate at the same concentration on AP were not different from each other significantly. Neither uridine triphosphate nor alpha,beta-methylene ATP had significant electrophysiologic effects on the sinoatrial node of rabbits. Both the electrophysiologic effects of ATP and Ado on pacemaker cells were inhibited by P1 receptor antagonist aminophylline 0.1 mmol/L (P<0.05) in a closely similar manner, and the effects of ATP were not affected by P2 receptor antagonist reactive blue 2 at 0.05 mmol/L (P>0.05).
CONCLUSION: There are no functional P2X(1) and P2Y(2) receptors on pacemaker cells of the rabbit sinoatrial nodes, and the electrophysiologic effects of ATP in the rabbit sinoatrial node pacemaker cells are mediated via P1 receptors by Ado degraded from ATP.