Long QT syndrome (LQTS) is commonly presented with life-threatening ventricular arrhythmias (VA). Renal artery denervation (RDN) is an alternative antiadrenergic treatment that attenuates sympathetic activity. We aimed to evaluate the efficacy of RDN on preventing VAs in LQTS rabbits induced by drugs. The subtypes of LQTS were induced by infusion of HMR-1556 for LQTS type 1 (LQT1), erythromycin for LQTS type 2 (LQT2), and veratridine for LQTS type 3 (LQT3). Forty-four rabbits were randomized into the LQT1, LQT2, LQT3, LQT1-RDN, LQT2-RDN, and LQT3-RDN groups. All rabbits underwent cardiac electrophysiology studies. The QTc interval of the LQT2-RDN group was significantly shorter than those in the LQT2 group (650.08 ± 472.67 vs. 401.78 ± 42.91 ms, p = 0.011). The QTc interval of the LQT3-RDN group was significantly shorter than those in the LQT3 group (372.00 ± 22.41 vs. 335.70 ± 28.21 ms, p = 0.035). The VA inducibility in all subtypes of the LQT-RDN groups was significantly lower than those in the LQT-RDN groups, respectively (LQT1: 9.00 ± 3.30 vs. 47.44 ± 4.21%, p < 0.001; LQT2: 11.43 ± 6.37 vs. 45.38 ± 5.29%, p = 0.026; LQT3: 10.00 ± 6.32 vs. 32.40 ± 7.19%, p = 0.006). This study demonstrated the neuromodulation of RDN leading to electrical remodeling and reduced VA inducibility of the ventricular substrate in LQT models.