AJP - Endo Watch the video to see how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Endocrinol Metab 273: E695-E700, 1997;
0193-1849/97 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tsuchida, K.
Right arrow Articles by Watajima, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tsuchida, K.
Right arrow Articles by Watajima, H.
Vol. 273, Issue 4, E695-E700, October 1997

Potassium currents in ventricular myocytes from genetically diabetic rats

Katsuharu Tsuchida and Hiroshi Watajima

Research Center, Taisho Pharmaceutical Company, Ohmiya, Saitama 330, Japan

Our previous study demonstrated the longer duration of action potential in ventricular myocytes from genetically diabetic WBN/Kob rats without change in calcium channel density compared with age-matched controls [Tsuchida, K., H. Watajima, and S. Otamo. Am. J. Physiol. 267 (Heart Circ. Physiol. 36): H2280-H2289, 1994]. In the present study we examined the alteration of potassium currents, especially transient outward current, in ventricular myocytes of genetically diabetic WBN/Kob rats. WBN/Kob rats gradually develop hyperglycemia with aging and show some similarity to non-insulin-dependent diabetes mellitus models, which differ from the insulin-dependent streptozotocin-treated rat model. The density of the intracellular calcium ion-independent transient outward current (Ito) from 17- to 19-mo diabetic rat myocytes was significantly smaller than that from age-matched control rat myocytes. In addition, the density of Ito from 17- to 19-mo rat myocytes was significantly less than that from 2-mo rat myocytes, suggesting that aging-induced alteration of Ito was accelerated by the diabetic state. The steady-state inactivation curves of Ito, the recovery from Ito inactivation, and the other outward currents were not significantly altered between diabetic myocytes and age-matched control myocytes. In conclusion, the prolonged duration of action potential from genetically diabetic rat myocytes is mainly due to the depressed Ito.

cardiomyocytes; transient outward current


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
Y. Zhang, J. Xiao, H. Wang, X. Luo, J. Wang, L. R. Villeneuve, H. Zhang, Y. Bai, B. Yang, and Z. Wang
Restoring depressed HERG K+ channel function as a mechanism for insulin treatment of abnormal QT prolongation and associated arrhythmias in diabetic rabbits
Am J Physiol Heart Circ Physiol, September 1, 2006; 291(3): H1446 - H1455.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
S. Jovanovic and A. Jovanovic
High Glucose Regulates the Activity of Cardiac Sarcolemmal ATP-Sensitive K+ Channels via 1,3-Bisphosphoglycerate: A Novel Link Between Cardiac Membrane Excitability and Glucose Metabolism
Diabetes, February 1, 2005; 54(2): 383 - 393.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
K. Dutta, D. A. Podolin, M. B. Davidson, and A. J. Davidoff
Cardiomyocyte Dysfunction in Sucrose-Fed Rats Is Associated With Insulin Resistance
Diabetes, May 1, 2001; 50(5): 1186 - 1192.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online