Abstract

We aimed to explore the effect of dibazol on the ophthalmic artery (OA) and ophthalmic artery smooth muscle cells (OASMCs) of C57BL/6J mice as well as the underlying mechanisms. The OA of C57BL/6J mice was isolated under a dissecting microscope for primary OASMCs culture and myogenic tests. OASMCs were identified through morphological and immunofluorescence analyses. Morphology changes in the OASMCs were examined by staining using rhodamine-phalloidin. We performed a collagen gel contraction assay to measure the contractile and relaxant activities of the OASMCs. The molecular probe Fluo-4 AM was used to examine intracellular free Ca 2+ levels ([Ca 2+ ] in ). The myogenic effects of OA were examined using wire myography . Additionally, the whole-cell patch-clamp technique was used to investigate the mechanisms underlying the relaxant effect of dibazol on L-type voltage-gated Ca 2+ channels (LVGC) in isolated cells. 10 −5  M dibazol significantly inhibited the contraction of OASMCs and increased the [Ca 2+ ] in response to 30 mM KCl in a concentration-dependent manner. Dizabol had a more significant relaxant effect than 10 −5  M isosorbide dinitrate (ISDN). Similarly, dibazol showed a significant dose-dependent relaxant effect on OA contraction induced by 60 mM KCl or 0.3 μM 9,11-Dideoxy-9α,11α-methanoepoxy prostaglandin F 2α (U46619). The current-voltage (I–V) curve revealed that dibazol decreased Ca 2+ currents in a concentration-dependent manner. In conclusion, dibazol exerted relaxant effects on the OA and OASMCs, which may involve the inhibition of the Ca 2+ influx through LVGC in the cells.