Electrophysiological and mechanical effects and alteration of intracellular Ca²⁺ concentration in canine ventricular muscle by amiloride, a potassium sparing diuretic
drug, were examined, using conventional microelectrode technique and fura-2 Ca²⁺-sensitive fluorescent dye. Amiloride (50 μM) depressed the action potential amplitude by 8.2±1.4% (n=8, P<0.05) and the maximum rate of depolarization by 16.2±2.0% (n=8, P<0.01). In addition, the action potential duration was prolonged by 26.7±3.4% (n=6, P<0.05) at 30 μM, and the resting potential was depolarized by 11.8±1.7% (n=6, P<0.05) at 0.5 mM amiloride. In contrast, amiloride (0.5 to 1 mM) significantly increased the
contractile force by 8 to 30% (n=8), but tended to decrease it at lower concentrations (30 μM to 0.1 mM). The positive inotropic effect was not affected by propranolol (0.1 μM), a β-adrenoceptor blocker. In fura-2 loaded ventricular myocytes, amiloride (1 mM) initially elevated cellular Ca²⁺ level ([Ca]₁) by 24.5±2.9% (n=6, P<0.01), and during the application, the [Ca]₁ level declined. These results indicate that amiloride possesses complex cardiac (protective) actions : electrical inhibitory and mechanical stimulatory actions, accompanied with the elevation of cellular Ca²⁺ concentration
