Vitamin K3 inhibits mouse uterine contraction in vitro via interference with the calcium transfer and the potassium channels

作者：Zhang, Xian-xia; Lu, Li-min; Wang, Li^*

来源：Biochemical and Biophysical Research Communications, 2016, 476(4): 393-399.

DOI：10.1016/j.bbrc.2016.05.132

• Vitamin K3
• Uterine contraction
• Calcium
• Potassium channel
• In vitro

Previous studies have demonstrated vitamin K3 had a great relief to smooth muscle spastic disorders, but no researches have yet pinpointed its possible anti-contractile activity in the uterus. Here, we evaluated the effect of vitamin K3 on myometrial contractility and explored the possible mechanisms of vitamin K3 action. Myograph apparatus were used to record the changes in contractility of isolated mouse uterine strips in a tissue bath. Uterine strips were exposed to vitamin K3 or vehicle. Vitamin K3 suppressed spontaneous contractions in a concentration dependent manner. It significantly decreased the contractile frequency induced by PGF2 alpha but not their amplitude (expect 58.0 mu M). Prior incubation with vitamin K3 reduced the effectiveness of PGF2 alpha-induced contraction. The antispasmodic effect of vitamin K3 was also sensitive to potassium channel blockers, such as tetraethylammonium, 4-aminopyridine, iberiotoxin) but not to the nitric oxide related pathway blockers. High concentrations (29.0, 58.0 mu M) of vitamin K3 weakened the Ca2+ dose response and inhibited phase 1 contraction (intracellular stored calcium release). These dates suggest that vitamin K3 specifically suppresses myometrial contractility by affecting calcium and potassium channels; thus, this approach has potential therapy for uterine contractile activity related disorders.

• 出版日期2016-8-5
• 单位复旦大学