Electrophysiologic effects of capsaicin on pacemaker cells in sinoatrial nodes of rabbits.
OBJECTIVE
To study the electrophysiologic effects of capsaicin on isolated pacemaker cells in sinoatrial (SA) nodes of rabbits and its possible action mechanism(s).


METHODS
Parameters of action potential (AP) in SA node were recorded using intracellular microelectrode technique.


RESULTS
By perfusion with capsaicin (10 micromol/L), the amplitude of action potential (APA) and maximal rate of depolarization (Vmax) were decreased from (55+/-4) mV to (49+/-4) mV (P<0.05) and from (2.4+/-0.5) V/s to (1.7+/-0.2) V/s (P<0.05). The velocity of diastolic (phase 4) depolarization (VDD) and rate of pacemaker firing (RPF) were decreased from (91+/-34) mV/s to (70+/-30) mV/s (P<0.01) and from (186+/-14) beat/min to (162+/-10) beat/min (P<0.01). The absolute value of maximal diastolic potential (MDP) was decreased from (49+/-3) mV to (44+/-2) mV (P<0.01). However, the duration of 90 % repolarization of action potential (APD90) was prolonged from (149+/-21) ms to (167+/-27) ms (P<0.01). Pretreatment with ruthenium red (RR, 10 micromol/L), a vanilloid receptor (VR1) blocker, did not affect the effects of capsaicin on SA node cells. Both elevation of calcium concentration (5 mmol/L) in superfusate and application of L-type Ca2+ channel agonist Bay-K-8644 (0.5 micromol/L) antagonized the effects of capsaicin on pacemaker cells. Beta-adrenergic agonist isoproterenol (Iso, 20 nmol/L) inhibited the capsaicin-induced prolongation of repolarization and decrease of MDP.


CONCLUSIONS
Capsaicin exerted a negative chronotropic action and induced a delayed repolarization of pacemaker cells in SA nodes of rabbits. These effects were likely due to reduction in calcium influx and/or potassium efflux, but were not mediated by VR1.
Cheng
Yan-Ping
YP
Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
Wang
Yi-He
YH
Cheng
Li-Ping
LP
He
Rui-Rong
RR
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002211:Capsaicin / Q000494:pharmacology*; D002469:Cell Separation; D005260:Female; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000502:physiology; D011817:Rabbits; D012849:Sinoatrial Node / Q000166:cytology*
D000318:Adrenergic beta-Agonists; D002120:Calcium Channel Agonists; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D007545:Isoproterenol; D002211:Capsaicin