ストレプトゾトシン糖尿病ラット心筋膜電位依存性カルシウムチャネル異常

抄録

To study possible Ca²⁺ overload into cardiac muscle, we measured the voltage-sensitive Ca²⁺ channel in cardiac muscle membrane fraction isolated from control and 10-wk-streptozocin-induced diabetic rats using [³H] PN 200-110, a dihydropyridine derivative, as a ligand. The maximum binding sites of [³H] PN 200-110 in cardiac membrane isolated from diabetic rats increased 61%(P<0.01) above that of the control without a significant change in Kd. Furthermore, [3H] PN 200-110 binding to control cardiac membrane was dose-dependently inhibited by verapamil, a phenylalkylamine Ca²⁺ antagonist, but such was not the case in cardiac membrane isolated from diabetic rats.
These results indicate both quantitative and qualitative changes in the voltage-sensitive Ca²⁺ channel and suggest another new mechanism for possible Ca²⁺ overload in the diabetic rat heart.