Repository logo
  • English
  • 中文
Log In
Have you forgotten your password?
  1. Home
  2. College of Medicine / 醫學院
  3. Toxicology / 毒理學研究所
  4. Use of ion channel blockers in the exploration of possible mechanisms involved in the myopathy of diabetic mice
 
  • Details

Use of ion channel blockers in the exploration of possible mechanisms involved in the myopathy of diabetic mice

Journal
Naunyn-Schmiedeberg's Archives of Pharmacology
Journal Volume
348
Journal Issue
3
Pages
311-318
Date Issued
1993
Author(s)
SHING-HWA LIU  
DOI
10.1007/BF00169161
URI
http://www.scopus.com/inward/record.url?eid=2-s2.0-0027179409&partnerID=MN8TOARS
http://scholars.lib.ntu.edu.tw/handle/123456789/301119
Abstract
Changes in the muscle contractions of the phrenic nerve-diaphragm preparation from the diabetic mouse were investigated by means of K+- and Cl--channel blockers and the Ca2+-mobilizing agent, selenite. The K+-channel blockers (UO22+ and 4-aminopyridine) cooperated synergistically with the Cl--channel blockers (Cd2+ and 9-anthracenecarboxylic acid) in increasing normal muscle contraction as described previously, but failed to induce this effect in the diaphragm of the diabetic mouse. Treatment with a Cl--channel blocker alone in 0.25 mmol/1 Ca2+ Krebs solution induced a myotonic activity accompanied by stimulus-bound repetitive action potential firings. This effect was also diminished in the diaphragm from diabetic mice. The membrane potential of the muscle cells in the diaphragm of the diabetic mouse was slightly but significantly decreased. The membrane input resistance was also increased and was refractory to being further increased by either a Cl--channel blocker or a low Cl--medium. Furthermore, the membrane chloride conductance was found to be decreased, but the membrane K+ conductance remained unchanged in the muscle from diabetic mice. These changes of membrane properties in the muscles from diabetic mice were shown to be similar to those induced by either Cl--channel blockers or a low Cl--medium. In addition, the combined treatment of the diaphragm from diabetic mice with Cd2+ Plus UO22+ in 0.25 mmol/l Ca2+ Krebs solution and then stepwise replenishment of Ca2+ led to a greater restoration of muscle contractions at a lower cumulative Ca2+ concentration than that was found with the normal diaphragm. The sustained muscle contracture of the mouse diaphragm induced by U022+ plus selenite was partially inhibited in the diaphragm from diabetic mice, indicating that the Ca2+ mobilizing mechanism of the diaphragm of the diabetic mouse was also altered. All of these observations obtained with the diaphragm of the diabetic mouse can be attributed to the diabetic state, because most of them could be normalized by insulin administration in vivo. Therefore, it is concluded that diabetes-induced changes of sarcolemmal ion channels and ion transporters may cause inhibition of muscle contraction and eventually lead to diabetic myopathy. ? 1993 Springer-Verlag.
Subjects
Alloxan diabetes; Ca2+ mobilization; Cl- conductance; Myopathy
SDGs

[SDGs]SDG3

Other Subjects
4 aminopyridine; 9 anthroic acid; alloxan; cadmium; chloride channel blocking agent; glucose; insulin; ion transport affecting agent; potassium channel blocking agent; sodium selenite; uranyl nitrate; alloxan diabetes mellitus; animal experiment; animal model; animal tissue; article; calcium mobilization; chloride conductance; controlled study; diaphragm; intracellular recording; ion transport; male; mouse; myopathy; nonhuman; phrenic nerve; priority journal; subcutaneous drug administration; Action Potentials; Animal; Blood Glucose; Body Weight; Cadmium; Chloride Channels; Diabetes Mellitus, Experimental; Insulin; Ion Channels; Male; Mice; Mice, Inbred ICR; Muscle Contraction; Muscular Diseases; Phrenic Nerve; Potassium Channels; Respiratory Muscles; Sodium Selenite; Support, Non-U.S. Gov't
Type
journal article

臺大位居世界頂尖大學之列,為永久珍藏及向國際展現本校豐碩的研究成果及學術能量,圖書館整合機構典藏(NTUR)與學術庫(AH)不同功能平台,成為臺大學術典藏NTU scholars。期能整合研究能量、促進交流合作、保存學術產出、推廣研究成果。

To permanently archive and promote researcher profiles and scholarly works, Library integrates the services of “NTU Repository” with “Academic Hub” to form NTU Scholars.

總館學科館員 (Main Library)
醫學圖書館學科館員 (Medical Library)
社會科學院辜振甫紀念圖書館學科館員 (Social Sciences Library)

開放取用是從使用者角度提升資訊取用性的社會運動,應用在學術研究上是透過將研究著作公開供使用者自由取閱,以促進學術傳播及因應期刊訂購費用逐年攀升。同時可加速研究發展、提升研究影響力,NTU Scholars即為本校的開放取用典藏(OA Archive)平台。(點選深入了解OA)

  • 請確認所上傳的全文是原創的內容,若該文件包含部分內容的版權非匯入者所有,或由第三方贊助與合作完成,請確認該版權所有者及第三方同意提供此授權。
    Please represent that the submission is your original work, and that you have the right to grant the rights to upload.
  • 若欲上傳已出版的全文電子檔,可使用Open policy finder網站查詢,以確認出版單位之版權政策。
    Please use Open policy finder to find a summary of permissions that are normally given as part of each publisher's copyright transfer agreement.
  • 網站簡介 (Quickstart Guide)
  • 使用手冊 (Instruction Manual)
  • 線上預約服務 (Booking Service)
  • 方案一:臺灣大學計算機中心帳號登入
    (With C&INC Email Account)
  • 方案二:ORCID帳號登入 (With ORCID)
  • 方案一:定期更新ORCID者,以ID匯入 (Search for identifier (ORCID))
  • 方案二:自行建檔 (Default mode Submission)
  • 方案三:學科館員協助匯入 (Email worklist to subject librarians)

Built with DSpace-CRIS software - Extension maintained and optimized by 4Science