title: Effect of dipfluzine on L-type calcium current in guinea pig ventricular myocytes.
abstract: OBJECTIVE
  To study the effect of dipfluzine (Dip) on L-type calcium current in guinea pig ventricular myocytes.
  
  
  METHODS
  Single myocytes were dissociated by enzymatic dissociation method. The current was recorded with the whole-cell configuration of the patch-clamp technique.
  
  
  RESULTS
  Dip (0.3 - 30 micromol/L) reduced the voltage-dependently activated peak value of I(Ca-L) in a concentration-dependent manner. The characteristics of I-V relationship were not greatly altered by Dip, and the maximal activation voltage of I(Ca-L) in the presence of Dip was not different from that of control. Steady-state activation of I(Ca-L) was not affected markedly, and the half activation potential V(0.5)) and the slope factor (kappa) in the presence of Dip 3 micromol/L were not markedly different from those of the control. V(0.5) value was (-12.8 +/- 1.7) mV in the control and (-13.2 +/- 2.4) mV in the presence of Dip 3 micromol/L. The kappa value was (7.1 +/- 0.4) mV in the control and (7.5 +/- 0.5) mV in the presence of Dip 3 micromol/L (n = 7 cells from 3 hearts, P > 0.05). Dip 3 micromol/L markedly shifted the steady-state inactivation curve of I(Ca-L) to the left, and accelerated the voltage-dependent steady-state inactivation of calcium current. V(0.5) value was (-19.7 +/- 2.4) mV in the control and (-31 +/- 6) mV in the presence of Dip 3 micromol/L. The kappa value was (3.6 +/- 0.3) mV in the control and (1.8 +/- 0.2) mV in the presence of Dip 3 micromol/L (n = 4 cells from 2 hearts, P < 0.05). Dip 3 micromol/L markedly delayed half-recovery time of Ca2+ channel from inactivation from (40 +/- 11) to (288 +/- 63) ms (n = 4, P < 0.01).
  
  
  CONCLUSIONS
  Dip mainly acts on the inactivated state of L-type calcium channel, accelerates the inactivation of calcium channel, and slows the recovery of calcium channel from inactivated state in guinea pig ventricular myocytes, through which the I(Ca-L) is inhibited.
authors.affiliation: Department of Physiology, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: Y J
authors.initials: YJ
authors.lastname: Zhang
authors.forename: D P
authors.initials: DP
authors.lastname: Li
authors.forename: B J
authors.initials: BJ
authors.lastname: Xue
authors.forename: Y L
authors.initials: YL
authors.lastname: Wang
authors.forename: R R
authors.initials: RR
authors.lastname: He
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D020746:Calcium Channels, L-Type / Q000187:drug effects*; D002469:Cell Separation; D002936:Cinnarizine / Q000031:analogs & derivatives* / Q000494:pharmacology*; D005260:Female; D006168:Guinea Pigs; D006352:Heart Ventricles; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D032383:Myocytes, Cardiac / Q000166:cytology* / Q000187:drug effects; D018408:Patch-Clamp Techniques
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D002936:Cinnarizine; C065758:dipfluzine