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Am J Physiol Endocrinol Metab 273: E695-E700, 1997;
0193-1849/97 $5.00
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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


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