Ginsenosides Rb1 and Re decrease cardiac contraction in adult rat ventricular myocytes: role of nitric oxide

Panax ginseng is used to enhance stamina and relieve fatigue as well as physical stress. Ginsenoside, the effective component of ginseng, regulates cardiovascular function. This study was to examine the effect of ginsenosides Rb1 and Re on cardiac contractile function at the cellular level. Ventricu...

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Bibliographic Details
Published in:British journal of pharmacology 2001-11, Vol.134 (6), p.1159-1165
Main Authors: Scott, Glenda I, Colligan, Peter B, Ren, Bonnie H, Ren, Jun
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Calcium - metabolism
Cardiovascular system
Dose-Response Relationship, Drug
General pharmacology
Ginsenoside Rb1 and Re
Ginsenosides
Heart Ventricles - drug effects
intracellular Ca2+ transients
Male
Medical sciences
Myocardial Contraction - drug effects
Myocardial Contraction - physiology
Myocardium - metabolism
myocyte shortening
NG-Nitroarginine Methyl Ester - pharmacology
nitric oxide
Nitric Oxide - metabolism
Nitric Oxide Synthase - metabolism
Panax
Pharmacognosy. Homeopathy. Health food
Pharmacology. Drug treatments
Rats
Rats, Sprague-Dawley
Saponins - chemistry
Saponins - pharmacology
Vasodilator agents. Cerebral vasodilators
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Summary:Panax ginseng is used to enhance stamina and relieve fatigue as well as physical stress. Ginsenoside, the effective component of ginseng, regulates cardiovascular function. This study was to examine the effect of ginsenosides Rb1 and Re on cardiac contractile function at the cellular level. Ventricular myocytes were isolated from adult rat hearts and were stimulated to contract at 0.5 Hz. Contractile properties analysed included: peak shortening (PS), time‐to‐90%PS (TPS), time‐to‐90% relengthening (TR90), and fluorescence intensity change (ΔFFI). Nitric oxide synthase (NOS) activity was determined by the 3H‐arginine to 3H‐citrulline conversion assay. Both Rb1 and Re exhibited dose‐dependent (1 – 1000 nM) inhibition in PS and ΔFFI, with maximal inhibitions between 20 – 25%. Concurrent application Rb1 and Re did not produce any additive inhibition on peak shortening amplitude (with a maximal inhibition of 24.9±6.1%), compared to Rb1 or Re alone. Pretreatment with the NOS inhibitor Nω‐nitro‐L‐arginine methyl ester (L‐NAME, 100 μM) abolished the effect of Rb1 and Re. Both Rb1 and Re significantly (P
ISSN:0007-1188
1476-5381
DOI:10.1038/sj.bjp.0704377