Transient Receptor Potential C4/5 Like Channel Is Involved in Stretch-Induced Spontaneous Uterine Contraction of Pregnant Rat.
10.4196/kjpp.2014.18.6.503
- Author:
Seungsoo CHUNG
1
;
Young Hwan KIM
;
Ji Hyun JOENG
;
Duck Sun AHN
Author Information
1. Department of Physiology, Yonsei University College of Medicine, Seoul 120-752, Korea. dsahn@yuhs.ac
- Publication Type:Original Article
- Keywords:
Osmotic stress;
Spontaneous uterine contraction;
Stretch;
Transient receptor potential C4/5
- MeSH:
Animals;
Female;
Gestational Age;
Humans;
Lanthanoid Series Elements;
Mice;
Muscle Cells;
Myometrium;
Obstetric Labor, Premature;
Osmotic Pressure;
Patch-Clamp Techniques;
Pregnancy;
Rats*;
Uterine Contraction*;
Uterus
- From:The Korean Journal of Physiology and Pharmacology
2014;18(6):503-508
- CountryRepublic of Korea
- Language:English
-
Abstract:
Spontaneous myometrial contraction (SMC) in pregnant uterus is greatly related with gestational age and growing in frequency and amplitude toward the end of gestation to initiate labor. But, an accurate mechanism has not been elucidated. In human and rat uterus, all TRPCs except TRPC2 are expressed in pregnant myometrium and among them, TRPC4 are predominant throughout gestation, suggesting a possible role in regulation of SMC. Therefore, we investigated whether the TRP channel may be involved SMC evoked by mechanical stretch in pregnant myometrial strips of rat using isometric tension measurement and patch-clamp technique. In the present results, hypoosmotic cell swelling activated a potent outward rectifying current in G protein-dependent manner in rat pregnant myocyte. The current was significantly potentiated by 1microM lanthanides (a potent TRPC4/5 stimulator) and suppressed by 10microM 2-APB (TRPC4-7 inhibitor). In addition, in isometric tension experiment, SMC which was evoked by passive stretch was greatly potentiated by lanthanide (1microM) and suppressed by 2-APB (10microM), suggesting a possible involvement of TRPC4/5 channel in regulation of SMC in pregnant myometrium. These results provide a possible cellular mechanism for regulation of SMC during pregnancy and provide basic information for developing a new agent for treatment of premature labor.
