Original Article

Effect of agmatine on L-type calcium current in rat ventricular myocytes.

Authors: Qing LI, Jing-Xiang YIN, Rui-Rong HE

Abstract

AIM: 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).
CONCLUSION: 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.
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