Guo-sheng Xiao1, Yu-hua Liao. 1. Department of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
Abstract
AIM: To investigate the effect of cilostazol on transient outward potassium current (I(to1) in isolated human atrial myocytes. METHODS: Atrial tissue samples were obtained from hearts of 15 patients ranging from 5 to 65 years of age (36.0 +/- 23.9 years). I(to1) was recorded by using the whole-cell patch clamp technique in enzymatically isolated atrial myocytes. RESULTS: Cilostazol at 30 micromol/ L significantly decreased I(to1) at the test potential of +50 mV. The peak amplitude of I(to1) was decreased from (8.16 +/- 0.70) pA/pF to (4.84 +/- 0.60) pA/pF (P < 0.01). In addition, the drug inhibited the current in a concentration-dependent manner (IC50 = 13.18 +/- 2.60 micromol/L). The significantly inhibitive effect was observed from the concentration of 1 micromol/L, and the maximal effect was 51.09% +/- 3.0% at 50 micromol/L. Furthermore, voltage-dependence of activation and inactivation, and time-dependent recovery from inactivation of I(to1) were not altered by cilostazol. CONCLUSION: The results indicates that cilostazol inhibits I(to1) in human atrial myocytes.
AIM: To investigate the effect of cilostazol on transient outward potassium current (I(to1) in isolated human atrial myocytes. METHODS: Atrial tissue samples were obtained from hearts of 15 patients ranging from 5 to 65 years of age (36.0 +/- 23.9 years). I(to1) was recorded by using the whole-cell patch clamp technique in enzymatically isolated atrial myocytes. RESULTS:Cilostazol at 30 micromol/ L significantly decreased I(to1) at the test potential of +50 mV. The peak amplitude of I(to1) was decreased from (8.16 +/- 0.70) pA/pF to (4.84 +/- 0.60) pA/pF (P < 0.01). In addition, the drug inhibited the current in a concentration-dependent manner (IC50 = 13.18 +/- 2.60 micromol/L). The significantly inhibitive effect was observed from the concentration of 1 micromol/L, and the maximal effect was 51.09% +/- 3.0% at 50 micromol/L. Furthermore, voltage-dependence of activation and inactivation, and time-dependent recovery from inactivation of I(to1) were not altered by cilostazol. CONCLUSION: The results indicates that cilostazol inhibits I(to1) in human atrial myocytes.
Authors: Amy C Sturm; Crystal F Kline; Patric Glynn; Benjamin L Johnson; Jerry Curran; Ahmet Kilic; Robert S D Higgins; Philip F Binkley; Paul M L Janssen; Raul Weiss; Subha V Raman; Steven J Fowler; Silvia G Priori; Thomas J Hund; Cynthia A Carnes; Peter J Mohler Journal: J Am Heart Assoc Date: 2015-05-26 Impact factor: 5.501