| Cheng, Y.W. and Kang, J.J. |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=None ------>paper_class3=2 ------>paper_class2=1 ------>vol= ------>confirm_bywho=kyhsu ------>insert_bywho=ywcheng ------>Jurnal_Rank=None ------>authors4_c=None ------>comm_author= ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=820 ------>medlineContent= ------>unit=000 ------>insert_date=20001004 ------>iam=1 ------>update_date= ------>author=??? ------>change_event=5 ------>ISSN=None ------>authors_c=None ------>score=473 ------>journal_name=British Journal of Pharmacology ------>paper_name=Emodin-induced muscle contraction of mouse diaphragm and the involvement Ca2+ influx and Ca2+ release from sarcoplasmic reticulum ------>confirm_date=20010725 ------>tch_id=089070 ------>pmid=9535008 ------>page1=815 ------>fullAbstract=1. The effects on skeletal muscle of emodin, an anthraquinone, were studied in the mouse isolated diaphragm and sarcoplasmic reticulum (SR) membrane vesicles. 2. Emodin dose-dependently caused muscle contracture, simultaneously depressing twitch amplitude. Neither tubocurarine nor tetrodotoxin blocked the contraction suggesting that it was caused myogenically. 3. The contraction induced by emodin persisted in a Ca2+ free medium with a slight reduction in the maximal force of contraction. The contraction induced by emodin in the Ca2+ free medium was completely blocked when the internal Ca2+ pool of the muscle was depleted by ryanodine. These data suggest that the contraction caused by emodin is due to the release of Ca2+ from the intracellular ryanodine-sensitive pool. 4. In contrast to the effect seen in the Ca2+ free medium, emodin induced a small but consisted contraction in the ryanodine-treated muscle in Krebs medium. The contraction was blocked in the presence of dithiothreitol and was partially blocked by nifedipine, suggesting that oxidation of a sulphhydryl group on the external site of dihydropyridine receptor is involved. 5. Emodin dose-dependently increased Ca2+ release from actively loaded SR vesicles and this effect was blocked by ruthenium red, a specific Ca2+ release channel blocker, and the thiol reducing agent, DTT, suggesting that emodin induced Ca2+ release through oxidation of the critical SH of the ryanodine receptor. 6. [3H]-ryanodine binding was dose-dependently potentiated by emodin in a biphasic manner. The degree of potentiation of ryanodine binding by emodin increased dose-dependently at concentrations up to 10 microM but decreased at higher concentrations of 10-100 microM. 7. These data suggest that muscle contraction induced by emodin is due to Ca2+ release from the SR of skeletal muscle, as a result of oxidation of the ryanodine receptor and influx of extracellular Ca2+ through voltage-dependent Ca2+ channels of the plasma membrane. ------>tmu_sno=None ------>sno=2430 ------>authors2=None ------>authors3=None ------>authors4=None ------>authors5=None ------>authors6=None ------>authors6_c=None ------>authors=Cheng, Y.W. and Kang, J.J. ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Emodin-induced muscle contraction of mouse diaphragm and the involvement of Ca2+ influx and Ca2+ release from sarcoplasmic reticulum. ------>language=2 ------>check_flag= ------>submit_date= ------>country=None ------>no=123 ------>patent_SDate=None ------>update_bywho= ------>publish_year=1998 ------>submit_flag= ------>publish_month=None |