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Effect of agmatine on L-type calcium current in rat ventricular myocytes.
Acta Pharmacol Sin. 2002 Mar; 23(3):219-24.AP

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.

Authors+Show Affiliations

Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11918845

Citation

Li, Qing, et al. "Effect of Agmatine On L-type Calcium Current in Rat Ventricular Myocytes." Acta Pharmacologica Sinica, vol. 23, no. 3, 2002, pp. 219-24.
Li Q, Yin JX, He RR. Effect of agmatine on L-type calcium current in rat ventricular myocytes. Acta Pharmacol Sin. 2002;23(3):219-24.
Li, Q., Yin, J. X., & He, R. R. (2002). Effect of agmatine on L-type calcium current in rat ventricular myocytes. Acta Pharmacologica Sinica, 23(3), 219-24.
Li Q, Yin JX, He RR. Effect of Agmatine On L-type Calcium Current in Rat Ventricular Myocytes. Acta Pharmacol Sin. 2002;23(3):219-24. PubMed PMID: 11918845.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of agmatine on L-type calcium current in rat ventricular myocytes. AU - Li,Qing, AU - Yin,Jing-Xiang, AU - He,Rui-Rong, PY - 2002/3/29/pubmed PY - 2003/9/17/medline PY - 2002/3/29/entrez SP - 219 EP - 24 JF - Acta pharmacologica Sinica JO - Acta Pharmacol Sin VL - 23 IS - 3 N2 - 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. SN - 1671-4083 UR - https://www.unboundmedicine.com/medline/citation/11918845/Effect_of_agmatine_on_L_type_calcium_current_in_rat_ventricular_myocytes_ DB - PRIME DP - Unbound Medicine ER -