title: Effect of agmatine on L-type calcium current in rat ventricular myocytes.
abstract: OBJECTIVE
  To study the effect of agmatine (Agm) on L-type calcium current (I(Ca-L)) in rat ventricular myocytes.
  
  
  METHODS
  Whole-cell configuration of the patch-clamp technique was used to record I(Ca-L) in single rat ventricular myocytes which were dissociated by enzymatic dissociation method.
  
  
  RESULTS
  (1) Agm (0.5, 1, 2 mmol/L) reduced the voltage-dependently activated peak amplitude of I(Ca-L) (pA) from 1451+/-236 (control) to 937+/-105 (n=8, P <0.05), 585+/-74 (n=8, P <0.01), and to 301+/-156 (n=8, P <0.01) in a concentration-dependent manner. (2) Agm (1 mmol/L) blocked I(Ca-L) in a use-dependent manner. The degree of use-dependent blocking effect was 53 %+/-12 % (n=8, P <0.05) at 1 Hz, and 69 %+/-11 % (n=8, P <0.01) at 3 Hz. (3) Agm upshifted the current-voltage (I-V) curve, but the characteristics of I-V relationship were not significantly altered by Agm, the maximal activation voltage of I(Ca-L) was not different from that of control. Steady-state activation of I(Ca-L) was not affected markedly. The half activation potential (V(0.5)) and the slope factor (k) were not significantly different from those of the control. V(0.5) value was (-20.2+/-2.5) mV in the control and (-20.5+/-2.7) mV in the presence of Agm 1 mmol/L. The k value was (7.1+/-0.4) mV and (7.5+/-0.5) mV, respectively (n=8, P >0.05). (4) Agm 1 mmol/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 (-32+/-6) mV in the control and (-40+/-5) mV in the presence of Agm. The k value was (7.6+/-0.9) mV and (12.5+/-1.1) mV, respectively (n=8, P <0.05). (5) Agm 1 mmol/L markedly delayed half-recovery time of Ca2+ channel from inactivation (92+/-28) ms to (249+/-26) ms (n=8, P <0.01).
  
  
  CONCLUSIONS
  Agm inhibited I(Ca-L) and mainly acted on the inactivated state of L-type calcium channel, manifested as acceleration of calcium channel inactivation and slowdown of recovery from inactivated state in rat ventricular myocytes.
authors.affiliation: Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: Qing
authors.initials: Q
authors.lastname: Li
authors.forename: Jing-Xiang
authors.initials: JX
authors.lastname: Yin
authors.forename: Rui-Rong
authors.initials: RR
authors.lastname: He
mesh_terms: D000376:Agmatine / Q000494:pharmacology*; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D020746:Calcium Channels, L-Type / Q000187:drug effects / Q000378:metabolism*; D002469:Cell Separation; D006352:Heart Ventricles / Q000166:cytology; D008839:Microelectrodes; D032342:Muscle Cells / Q000187:drug effects* / Q000378:metabolism; D018408:Patch-Clamp Techniques; D051381:Rats
chemical_list: D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D000376:Agmatine