scholarly journals Estrogen dependence of the renal vasodilatory effect of nicotine in rats: Role of α7 nicotinic cholinergic receptor/eNOS signaling

Life Sciences ◽  
2011 ◽  
Vol 88 (3-4) ◽  
pp. 187-193 ◽  
Author(s):  
Mahmoud M. El-Mas ◽  
Sahar M. El-gowilly ◽  
Eman Y. Gohar ◽  
Abdel-Rheem M. Ghazal ◽  
Abdel A. Abdel-Rahman
Nature ◽  
1981 ◽  
Vol 293 (5833) ◽  
pp. 580-583 ◽  
Author(s):  
K. Whaley ◽  
D. Lappin ◽  
T. Barkas

Genes ◽  
2016 ◽  
Vol 7 (11) ◽  
pp. 95 ◽  
Author(s):  
Lingjun Zuo ◽  
Rolando Garcia-Milian ◽  
Xiaoyun Guo ◽  
Chunlong Zhong ◽  
Yunlong Tan ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Hong Ping Zhang ◽  
Dan-Dan Zhang ◽  
Yan Ke ◽  
Ka Bian

Inflammation plays a pivotal role in the development and progression of cardiovascular diseases, in which, the endothelium dysfunction has been a key element. The current study was designed to explore the vasodilatory effect of anti-inflammatory herbs which have been traditionally used in different clinical applications. The total saponins fromActinidia argutaradix (SAA), total flavonoids fromGlycyrrhizaeradix et rhizoma (FGR), total coumarins fromPeucedaniradix (CPR), and total flavonoids fromSpatholobicaulis (FSC) were extracted. The isometric measurement of vasoactivity was used to observe the effects of herbal elements on the isolated aortic rings with or without endothelium. To understand endothelium-independent vasodilation, the effects of herb elements on agonists-induced vasocontractility and on the contraction of endothelium-free aortic rings exposed to a Ca2+-free medium were examined. Furthermore, the role of nitric oxide signaling in endothelium-dependent vasodilation was also evaluated. In summary, FGR and FSC exhibit potent anti-inflammatory effects compared to CPR and SAA. FGR exerts the strongest vasodilatory effect, while CPR shows the least. The relaxation induced by SAA and FSC required intact endothelia. The mechanism of this vasodilation might involve eNOS. CPR-mediated vasorelaxation appears to involve interference with intracellular calcium homeostasis, blocking Ca2+influx or releasing intracellular Ca2+.


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