title: Vitamin K3 inhibits mouse uterine contraction in vitro via interference with the calcium transfer and the potassium channels.
abstract: 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 PGF2ɑ but not their amplitude (expect 58.0 μM). Prior incubation with vitamin K3 reduced the effectiveness of PGF2ɑ-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 μM) of vitamin K3 weakened the Ca(2+) 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.
authors.affiliation: Shanghai OB/GYN Hospital, Fudan University, Shanghai 200011, China; Department of Obstetrics and Gynecology of Shanghai Medical College, Fudan University, Shanghai 200032, China. Electronic address: zxx19881222@126.com.
authors.forename: Xian-Xia
authors.initials: XX
authors.lastname: Zhang
authors.affiliation: Department of Physiology and Pathophysiology, Shanghai Medical College, Fudan University, Shanghai 200032, China. Electronic address: lulimin@shmu.edu.cn.
authors.forename: Li-Min
authors.initials: LM
authors.lastname: Lu
authors.affiliation: Shanghai OB/GYN Hospital, Fudan University, Shanghai 200011, China; Shanghai Key Laboratory of Female Reproductive Endocrine-Related Diseases, Shanghai 200011, China; Department of Obstetrics and Gynecology of Shanghai Medical College, Fudan University, Shanghai 200032, China. Electronic address: wanglisa1101@126.com.
authors.forename: Li
authors.initials: L
authors.lastname: Wang
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D015237:Dinoprost / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005260:Female; D051379:Mice; D009213:Myography / Q000379:methods; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009924:Organ Culture Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000378:metabolism*; D014590:Uterine Contraction / Q000187:drug effects* / Q000502:physiology; D024483:Vitamin K 3 / Q000494:pharmacology*
chemical_list: D015220:Calcium Channels; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D024483:Vitamin K 3; D015237:Dinoprost; D002118:Calcium; D019331:NG-Nitroarginine Methyl Ester
keywords: Calcium; In vitro; Potassium channel; Uterine contraction; Vitamin K3