Electrophysiological effects of capsaicin on spontaneous activity of rabbit atrioventricular node cells.
- Author:
Qian LI
1
;
Yu-Ming WU
;
Rui-Rong HE
Author Information
1. Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017 China.
- Publication Type:Journal Article
- MeSH:
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester;
pharmacology;
Action Potentials;
drug effects;
Animals;
Atrioventricular Node;
cytology;
physiology;
Calcium;
metabolism;
Calcium Channel Agonists;
pharmacology;
Calcium Channels, L-Type;
drug effects;
Capsaicin;
pharmacology;
Male;
Microelectrodes;
Rabbits;
Receptors, Drug;
antagonists & inhibitors;
Ruthenium Red;
pharmacology
- From:
Acta Physiologica Sinica
2004;56(2):248-252
- CountryChina
- Language:English
-
Abstract:
To study the electrophysiological effects of capsaicin on spontaneous activity of rabbit atrioventricular (AV) node cells, parameters of action potential in AV node were recorded using intracellular microelectrode technique. Capsaicin (1-30 micromol/L) not only decreased the amplitude of action potential, maximal rate of depolarization (V(max)), velocity of diastolic (phase 4) depolarization, and rate of pacemaker firing, but also prolonged the duration of 90% repolarization of action potential (APD(90)) in a concentration-dependent manner. Both application of L-type Ca(2+) channel agonist Bay K8644 (0.5 micromol/L) and elevation of calcium concentration (5 mmol/L) in superfusate antagonized the effects of capsaicin on pacemaker cells. Pretreatment with ruthenium red (10 micromol/L), a capsaicin receptor blocker, did not affect the effects of capsaicin on AV node cells. Capsaicin exerted an inhibitory action on spontaneous activity of AV node cells in rabbits. These effects were likely due to reduction in calcium influx, but were not mediated by VR1.
