Role of nitric oxide in ginsenoside Rg(1)-induced protection against left ventricular hypertrophy produced by abdominal aorta coarctation in rats.
Ginsenoside Rg(1) (Rg(1)), one of the active components of Panax ginseng, has been reported to promote endogenous nitric oxide (NO) production in some tissues, and to inhibit left ventricular (LV) hypertrophy in rats. This study aimed to investigate whether Rg(1)-induced inhibition of rat LV hypertrophy is mediated by NO-production. Rat LV hypertrophy was induced by abdominal aorta coarctation. Rg(1) 15 mg/kg/d, L-arginine 200 mg/kg/d, and the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine-methyl ester (L-NAME) 100 mg/kg/d used with the same dose of L-arginine or Rg(1) were given starting from 1 d after surgery for 21 consecutive days. LV hypertrophy was evidenced by determining LV weight and mRNA expression of atrial natriuretic peptide, a marker of cardiac hypertrophic response, as well as by histopathology. Rg(1) and L-arginine administration significantly reduced the elevated LV hypertrophic parameters independent of LV systolic pressure changing, and ameliorated the histopathology of LV myocardium and LV diastolic function. All the beneficial effects of Rg(1) and L-arginine were abolished or blunted by L-NAME. Further to examine the role of NO in Rg(1) inhibition on LV hypertrophy, expression of endothelial NOS was determined at the transcript levels. In our experimental conditions endothelial NOS mRNA expression in LV tissue was lowered by abdominal aorta coarctation, and upregulated by Rg(1) administration. These results demonstrate that Rg(1)-induced protection against LV hypertrophy elicited by abdominal aorta coarctation in rats is mediated, at least in part, via endogenous NO production and release.
Deng
Jiang
J
Department of Pharmacology, Zunyi Medical College, China.
Wang
Yi-Wei
YW
Chen
Wen-Ming
WM
Wu
Qin
Q
Huang
Xie-Nan
XN
D000005:Abdomen / Q000098:blood supply; D000818:Animals; D001017:Aortic Coarctation; D001120:Arginine / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000235:genetics / Q000378:metabolism; D002317:Cardiovascular Agents / Q000494:pharmacology / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004727:Endothelium / Q000201:enzymology; D036145:Ginsenosides / Q000494:pharmacology / Q000627:therapeutic use*; D006352:Heart Ventricles / Q000187:drug effects* / Q000473:pathology; D017379:Hypertrophy, Left Ventricular / Q000188:drug therapy*; D008297:Male; D009206:Myocardium / Q000473:pathology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000096:biosynthesis*; D019001:Nitric Oxide Synthase / Q000235:genetics / Q000378:metabolism; D009929:Organ Size; D005894:Panax / Q000737:chemistry*; D008517:Phytotherapy; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
D002317:Cardiovascular Agents; D036145:Ginsenosides; D012333:RNA, Messenger; D009569:Nitric Oxide; D009320:Atrial Natriuretic Factor; D001120:Arginine; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester