Potassium currents in ventricular myocytes from genetically diabetic rats. Tsuchida, Katsuharu, and Hiroshi Watajima. Research Center, Taisho Pharmaceutical Co., Ltd., Ohmiya, Saitama 330, Japan
APStracts 4:0127E, 1997.
Our previous study demonstrated the longer duration of action potential in ventricular myocytes from genetically diabetic WBN/Kob rats without calcium channel density compared with age-matched controls (Am. J. Physiol. 267 : 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 noninsulin-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 17-19 mo diabetic rat myocytes was significantly smaller than that from age -matched control rat myocytes. In addition, the density of Ito from 17-19 mo rat myocytes was significantly smaller 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. 

Received 25 February 1997; accepted in final form 4 June 1997.
APS Manuscript Number E87-7.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 1 July 1997