Catharanthus roseus is a traditional herbal medicine used in Asian and African 
countries for the treatment of various diseases including hypertension. The 
present study examined possible cellular mechanisms for the relaxation of rat 
renal arteries induced by vindorosine extracted from C. roseus. Intrarenal 
arteries were isolated from 200-300 g male Sprague-Dawley rats and treated with 
different pharmacological blockers and inhibitors for the measurement of 
vascular reactivity on a Multi Myograph System. Fluorescence imaging by laser 
scanning confocal microscopy was utilized to determine the intracellular Ca(2+) 
level in the vascular smooth muscles of the renal arteries. Vindorosine in 
micromolar concentrations relaxes renal arteries precontracted by KCl, 
phenylephrine, 11-dideoxy-9α,11α-epoxymethanoprostaglandin F2α, and serotonin. 
Vindorosine-induced relaxations were unaffected by endothelium denudation or by 
treatment with the nitric oxide synthase inhibitor N (G)-nitro-L-arginine methyl 
ester hydrochloride, the guanylyl cyclase inhibitor 
1H-[1, 2, 4]oxadiazolo[4,3-a]quinoxalin-1-one, the cyclooxygenase inhibitor 
indomethacin, or K(+) channel blockers such as tetraethylammonium ions, 
glibenclamide, and BaCl2. Vindorosine-induced relaxations were attenuated in the 
presence of 0.1 µM nifedipine (an L-type Ca(2+) channel blocker). Vindorosine 
also concentration-dependently suppressed contractions induced by CaCl2 
(0.01-5 mM) in Ca-free 60 mM KCl solution. Furthermore, fluorescence imaging 
using fluo-4 demonstrated that 30 min incubation with 100 µM vindorosine reduced 
the 60 mM KCl-stimulated Ca(2+) influx in the smooth muscles of rat renal 
arteries. The present study is probably the first report of blood vessel 
relaxation by vindorosine and the possible underlying mechanisms involving the 
inhibition of Ca(2+) entry via L-type Ca(2+) channels in vascular smooth 
muscles.