Electrophysiological Effects of Purinergic Receptor Agonists on Atrial Muscle Fiber under Normal and Ischemic Conditions.
10.4070/kcj.1994.24.4.645
- Author:
Jae Ha KIM
;
Byoung Hee AHN
;
Jung Chaee KANG
- Publication Type:In Vitro ; Original Article
- Keywords:
Purinoceptor;
Ischemia;
Rat atrium
- MeSH:
Action Potentials;
Adenosine;
Adenosine Triphosphate;
Animals;
Ischemia;
Microelectrodes;
Molar;
Purinergic Agonists*;
Rats;
Receptors, Purinergic
- From:Korean Circulation Journal
1994;24(4):645-654
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: The electrophysiological effects of purinergic receptor agonists, adenosine triphosphate(ATP) and adenosine were examined using conventional microelectrode technique in rat atrial muscle fibers under superfused with a normal or a simulated ischemic(hypoxic, hyperkalemic and acidotic) physiologic salt solution(PSS) in vitro. METHODS: Action potential parameters, such as maximal diastolic potential(MDP), action potential amplitude(APA), rate of phase 0 depolarization(dv/dtmax) and action potential duration(APD90) were measured in electrically paced, physiologic salt solution(Tyrode's) superfused left rat atrium. In the experiment of ischemic simulation in vitro, normal physiologic salt solutions(NPSS0 were modified(MPSS) and superfused in substitute for normal Tyrode's solution. To investigate the effects of purinergic receptor agonists, ATP or adenosine was added to the superfused tyrode's solutions(NPSS or MPSS) in molar concentration. RESULTS: Under superfused with normal PSS, ATP(10(-3), 10(-4)M) elicited slight hyperpolarization in MDP, and both ATP(10(-6)-10(-3)M) and adenosine(10(-6)-10(-3)M) shortened the duration of normal action potential in a dose-dependent manner. The other paramaters were not affected by the drugs. Superfusion with ischemic PSS caused reductions in MDP as well as APA, dv/dtmax and, especially, APD90. The effects produced by the initial 10 minutes of superfusion with ischemic PSS almost completely disappeared during a subsequent period of continued superfusion with normal PSS, but, those by the initial 20 min lasted in some degree. Both ATP(10(-4)M) and adenosine(10(-4)M) attenuated the reduction in the rate of phase 0 depolarization and the amplitude of the action potential amplitude produced by the ischemic PSS. CONCLUSION: Purinergic receptor agonists, ATP and adensoine, caused a concentration-dependent shortening of the action potential duration in rat atrial muscle fibers and they attenuated the reductions in the rate of phase 0 depolarization and action potential amplitude in fibers superfused with ischemic PSS.
