Electrophysiologic effects of capsaicin on pacemaker cells in sinoatrial nodes of rabbits
Abstract
AIM: 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.
CONCLUSION: 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.
Keywords:
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.
CONCLUSION: 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.