Tetracaine

Tetracaine (Amethocaine) is a sodium channel inhibitor and ryanodine receptor (RyR) inhibitor. Tetracaine blocks sodium conduction across nerve cell membranes, preventing rapid sodium ion influx and depolarization. Tetracaine exhibits biphasic effects on spontaneous sarcoplasmic reticulum Ca²⁺ release in Ca²⁺-overloaded ventricular myocytes, and increases sarcoplasmic reticulum Ca²⁺ load. Tetracaine can be used in research related to eye diseases^[1][2][3].
In Vitro:Tetracaine inhibits human NaV1.7 channel with IC₅₀ values of 0.11 μM (V_hold = -65 mV) and 0.62 μM (V_hold = -90 mV), respectively, and shows >300-fold reduced potency against the NaV1.7^F1737A mutant channel^[1].
Tetracaine (V_hold = -90 mV) inhibits human NaV1.5 channel with an IC₅₀ value of 0.53 μM^[1].
Tetracaine (V_hold = -65 mV) inhibits human NaV1.2 channel with an IC₅₀ value of 1.1 μM^[1].
Tetracaine exerts biphasic effects on spontaneous Ca²⁺ release in Ca²⁺-overloaded rat ventricular myocytes, initially inhibiting Ca²⁺ sparks and waves at concentrations >0.25 mM, then potentiating release at submaximal concentrations (<1.25 mM), while completely abolishing release at ≥1.5 mM^[3].
Tetracaine (0.75 mM; 2-5 min) causes a time-dependent increase in SR Ca²⁺ load in Ca²⁺-overloaded rat ventricular myocytes, with a 19% increase after 2 min and a 54% increase after 5 min of exposure^[3].
Tetracaine (0.75 mM; up to 10 min) has delayed potentiation of spontaneous Ca²⁺ release in rat ventricular myocytes that depends on extracellular Ca²⁺ concentration^[3].
Tetracaine (1 mM) enhances net Ca²⁺ uptake in isolated canine cardiac SR microsomes by reducing Ca²⁺ leakage through RyR channels^[3].
Tetracaine inhibits canine cardiac SR RyR channel activity in planar lipid bilayers with an EC₅₀ of 0.26 mM at low luminal Ca²⁺, and this inhibition is reversed by elevated luminal Ca^2+[3].