A Carbohydrate Fraction, AIP1, from Artemisia Iwayomogi Reduces the Action Potential Duration by Activation of Rapidly Activating Delayed Rectifier K+ Channels in Rabbit Ventricular Myocytes.
10.4196/kjpp.2010.14.3.119
- Author:
Won Sun PARK
1
;
Youn Kyoung SON
;
Eun A KO
;
Seong Woo CHOI
;
Nari KIM
;
Tae Hoon CHOI
;
Hyun Joo YOUN
;
Su Hyun JO
;
Da Hye HONG
;
Jin HAN
Author Information
1. Department of Physiology, Institute of Medical Science, Kangwon National University School of Medicine, Chuncheon 200-701, Korea.
- Publication Type:Original Article
- Keywords:
Artemisia iwayomogi;
Delayed rectifier K+ current;
Long QT syndrome;
Ventricular myocyte
- MeSH:
Action Potentials;
Artemisia;
Asteraceae;
Chromans;
Diphosphonates;
Heart Rate;
Humans;
Ion Channels;
Long QT Syndrome;
Membrane Potentials;
Muscle Cells;
Piperidines;
Plants;
Pyridines;
Sulfonamides
- From:The Korean Journal of Physiology and Pharmacology
2010;14(3):119-125
- CountryRepublic of Korea
- Language:English
-
Abstract:
We investigated the effects of a hot-water extract of Artemisia iwayomogi, a plant belonging to family Compositae, on cardiac ventricular delayed rectifier K+ current (I(K)) using the patch clamp technique. The carbohydrate fraction AIP1 dose-dependently increased the heart rate with an apparent EC(50) value of 56.1+/-5.5 microgram/ml. Application of AIP1 reduced the action potential duration (APD) in concentration-dependent fashion by activating I(K) without significantly altering the resting membrane potential (IC(50) value of APD(50): 54.80+/-2.24, IC(50) value of APD(90): 57.45+/-3.47 microgram/ml). Based on the results, all experiments were performed with 50 microgram/ml of AIP1. Pre-treatment with the rapidly activating delayed rectifier K+ current (I(Kr)) inhibitor, E-4031 prolonged APD. However, additional application of AIP1 did not reduce APD. The inhibition of slowly activating delayed rectifier K+ current (I(Ks)) by chromanol 293B did not change the effect of AIP1. AIP1 did not significantly affect coronary arterial tone or ion channels, even at the highest concentration of AIP1. In summary, AIP1 reduces APD by activating I(Kr) but not I(Ks). These results suggest that the natural product AIP1 may provide an adjunctive therapy of long QT syndrome.
