Effects of RP58866 on transmembrane K+ currents in mammalian ventricular myocytes.
Zhongguo Yao Li Xue Bao
; 20(11): 961-9, 1999 Nov.
Article
em En
| MEDLINE
| ID: mdl-11270975
ABSTRACT
AIM:
To determine effects of RP58866 on inward rectifier K+ current (IKl), transient outward K+ current (Ito) and delayed outward rectifier K+ current (IK) in isolated cardiac myocytes.METHODS:
In isolated ventricular myocytes of guinea pig and dog, the effect of RP58866 on IKl, Ito, and IK were observed by the whole cell voltage-clamp technique.RESULTS:
RP58866 decreased IKl in a concentration-dependent manner, with an IC50 of (3.4 +/- 0.8) micromol.L-1 (n = 6) at -100 mV in guinea pig ventricular cells. In dog ventricular myocytes, RP58866 inhibited Ito with IC50 of (2.3 +/- 0.5) micromol.L-1 at +40 mV. In guinea pig ventricular cells, RP58866 at 100 micromol.L-1 decreased IK IKstep by (58 +/- 13)% at +40 mV, and IKtail by (86 +/- 17)%, respectively. RP58866 inhibited IKstep with an IC50 of (7.5 +/- 0.8) micromol.L-1, and IKtail with an IC50 of (3.5 +/- 0.9) micromol.L-1. The envelope of tail analysis suggested that both IKr and IKs were inhibited.CONCLUSION:
RP58866 inhibits IKl, Ito, and IK in cardiac myocytes with a similar potency, and is not a specific IKl inhibitor.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Piperidinas
/
Canais de Potássio
/
Cromanos
/
Antiarrítmicos
/
Miocárdio
Limite:
Animals
Idioma:
En
Ano de publicação:
1999
Tipo de documento:
Article