Aim To examine whether L-type calcium channel （LCC） of human umbilical arterial smooth muscle cells （HUASMC） was influenced by endothelin-1（ET-1）, and whether the possible influence was interfered with by quercetin which has been shown to provide protection against cardiovascular diseases. Methods Primary HUASMC at the third passage culture were identified by immunocytochemistry and randomly divided into following groups:①control group: cultured only with vehicle for 24 h. ② Quercetin alone group: cultured with 80 μmol/L quercetin for 24 h. ③Model group: cultured with 10 nmol/L ET-1 for 24 h. ④U0126 plus ET-1 group: pretreated with 10 μmol/L U0126 for 1 h, then coincubated with 10 nmol/L ET-1 for 24 h. ⑤Quercetin pretreatment group: pretreated with quercetin in concentrations of 20 μmol/L, 40 μmol/L and 80 μmol/L respectively for 1 h, then coincubated with 10 nmol/L ET-1 for another 24 h. ⑥ET-1+Que+U0126 group: pretreated with 80 μmol/L quercetin and 10 μmol/L U0126 together for 1 h, then coincubated with 10 nmol/L ET-1 for 24 h. ⑦ET-1+nifedipine group: pretreated with 10 μmol/L nifedipine for 1 h, then coincubated with 10 nmol/L ET-1 for 24 h. Expression of α_1C, a LCC major subunit , was assayed by RT-PCR and Western blot analysis. The LCC currents（ICaL） were detected by technique of whole-cell patch-clamp. Results α_1C expression , in both mRNA and protein level, as well as ICaL density of model group were significantly down-regulated compared with that of control group or quercetin alone group（P<0.05）, and the repressing effect of ET-1 on LCC was partly reversed by pretreating with U0126 or quercetin（P<0.05）. No significant difference between control group and quercetin alone group was detected. Conclusion Downregulation of α_1C expression and ICaL density in HUASMC by ET-1 partly via ERK parthway was antagonized by quercetin, which could be an important mechanism contributing to the protective effect of quercetin on cardiovascular system.