Germinated Buckwheat extract decreases blood pressure and nitrotyrosine immunoreactivity in aortic endothelial cells in spontaneously hypertensive rats

2009 ◽  
Vol 23 (7) ◽  
pp. 993-998 ◽  
Author(s):  
Dae Won Kim ◽  
In Koo Hwang ◽  
Soon Sung Lim ◽  
Ki-Yeon Yoo ◽  
Hua Li ◽  
...  
PLoS ONE ◽  
2014 ◽  
Vol 9 (2) ◽  
pp. e90339 ◽  
Author(s):  
Rocío Salsoso ◽  
Enrique Guzmán-Gutiérrez ◽  
Pablo Arroyo ◽  
Carlos Salomón ◽  
Sonia Zambrano ◽  
...  

2020 ◽  
Vol 15 (1) ◽  
pp. 1934578X1990071
Author(s):  
Harsha Nagar ◽  
Shin Kwang Kang ◽  
Si Wan Choi ◽  
Hee-Jung Song ◽  
Su-Jeong Choi ◽  
...  

Ginseng is well known to treat various diseases. Ginsenoside Rg3 exhibits a variety of pharmacological activities including cardiovascular protective effects. Vitamins utilized as supplements have minimal interactions with other drugs making them attractive targets for therapeutics. Here, we prepared Rg3-enriched Korean ginseng catalyzed by vitamin (REKVG) and evaluated its ability to improve hypertension in spontaneously hypertensive rats (SHRs). The ginsenoside content in both Korean Red ginseng (KRG) and REKVG were analyzed using high-performance liquid chromatography (HPLC). Male SHRs and Wistar-Kyoto rats (WKYs) were randomly divided into 6 groups (WKY saline, WKY KRG, WKY REKVG, SHR saline, SHR KRG, and SHR REKVG). KRG and REKVG were orally administered once daily to the rats at a dose of 10 mg/kg for 6 weeks, and blood pressure was measured in live rats using the tail-cuff method. Human umbilical vein endothelial cells were used for the in vitro experiment. HPLC chromatograms revealed that the concentration of ginsenoside Rg3 in REKVG was much higher than that in KRG. The administration of REKVG significantly decreased the systolic blood pressure in SHRs at the end of 6 weeks as compared to KRG. Further, REKVG use resulted in a dose-dependent increase in Akt and endothelial nitric oxide synthase (eNOS) phosphorylation and NO production in endothelial cells. In addition, the administration of REKVG significantly increased Akt and eNOS phosphorylation and increased plasma NO levels in SHRs. We conclude that REKVG effectively lowers the blood pressure in rats and therefore could be considered for use in preventing or improving hypertension.


1992 ◽  
Vol 263 (5) ◽  
pp. R1035-R1041
Author(s):  
K. Yokokawa ◽  
A. K. Mandal ◽  
M. Kohno ◽  
T. Horio ◽  
K. Murakawa ◽  
...  

Previous studies have shown that chronic subcutaneous administration of heparin significantly reduces blood pressure in hypertensive rats. The intracellular mechanisms of how heparin prevents smooth muscle cell proliferation remain unclear. This study was designed to examine whether heparin affects endothelin-1 action and production, to further elucidate the mechanism of the antihypertensive effect of heparin. Four-week treatment with heparin (300 U/day sc) significantly decreased blood pressure in spontaneously hypertensive rats (SHR; 199 +/- 8 vs. 164 +/- 9 mmHg; P < 0.001) and completely blunted pressor response to endothelin-1 in SHR. Heparin treatment did not decrease blood pressure response nor did it attenuate blood pressure responses to endothelin-1 in Wistar-Kyoto rats (WKY). Heparin significantly suppressed endothelin-1-induced increase in intracellular calcium concentration and inositol 1,4,5-trisphosphate level in cultured vascular smooth muscle cells in a dose-dependent manner and endothelin-1 release from cultured endothelial cells. These inhibitions were significantly more pronounced in SHR than in WKY. In conclusion, our findings indicate that the antihypertensive effect of heparin is mediated, at least in part, by the inhibition of endothelin-1 action on vascular smooth muscle cells and endothelin-1 production from endothelial cells.


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