1. Extracts of Ginkgo biloba (EGb) and ginsenosides (GS) have been reported to induce vasorelaxation. In the present study, the role of K+ channels in the action of EGb and GS to activate nitric oxide synthase (NOS) activity was investigated in cultured endothelial cells. 2. Nitric oxide synthase activity of cultured endothelial cells detected by the reduced nicotinamide adenine dinucleotide phosphate (NADPH) histochemistry method was significantly increased after treatment with 20 μg/mL EGb or 40 μg/mL GS plus 10 mmol/L L-arginine. The effect was completely abolished by the addition of 0.5 μmol/L Nω-nitro-L-arginine, an inhibitor of NOS, to the incubation medium and partially inhibited by 10 μmol/L tetraethylammonium (TEA), an inhibitor of Ca2+-activated K+ (KCa) channels. 3. Application of EGb to the intracellular surface of excised inside-out patches activated K+ channels in a concentration-dependent manner in the concentration range 1-100 μg/mL. Channel activity was also activated by application of GS at concentrations ranging from 1 to 300 μg/mL. The modulation of channel activity was inhibited by 0.5 mmol/L TEA but not by 0.5 mmol/L glibenclamide, an inhibitor of ATP-sensitive K+ channels. 4. Thus, in cultured endothelial cells, the increase in NOS activity induced by EGb or GS depends on the activity of KCa channels. These compounds may regulate nitric oxide release by changing the cell membrane potential in vascular endothelial cells.
|Number of pages||5|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|Publication status||Published - 2001|
All Science Journal Classification (ASJC) codes
- Physiology (medical)