In streptozotocin-induced diabetic mice, the reduced alpha-adrenoceptor-mediated negative inotropy is partly due to pathological prolongation of the action potential duration.
Does pathological prolongation of action potential duration cause reduced alpha-adrenoceptor-mediated negative inotropy in streptozotocin-induced diabetic mice myocardium?
Prolonged action potential duration contributes to the reduced alpha-adrenoceptor-mediated negative inotropy observed in diabetic mouse myocardium.
Effect of pathological prolongation of action potential duration on the α-adrenoceptor-mediated negative inotropy was studied in streptozotocin-induced diabetic mice myocardium. In streptozotocin-treated mouse ventricular myocardium, which had longer duration of action potential than that in control mice, the negative inotropic response induced by phenylephrine was smaller than that in control mice. 4-Aminopyridine prolonged the action potential duration and decreased the negative inotropy in control mice. Cromakalim shortened the action potential duration and increased the negative inotropy in streptozotocin-treated mice. These results suggest that the reduced α-adrenoceptor-mediated inotropy in the diabetic mouse myocardium is partly due to its prolonged action potential.
Kanae et al. (Tue,) conducted a other in Streptozotocin-induced diabetes. Phenylephrine, 4-Aminopyridine, Cromakalim vs. Control mice was evaluated on α-adrenoceptor-mediated negative inotropy and action potential duration. In streptozotocin-induced diabetic mice, the reduced alpha-adrenoceptor-mediated negative inotropy is partly due to pathological prolongation of the action potential duration.