Objectives: Tamsulosin is a common α1-AR antagonist that is prescribed to patients with acute kidney stone episodes. According to accumulated experimental data, abnormal peristaltic contraction of the ureter smooth muscle (USM) causes acute kidney stone episodes. Transient Potassium channels (KA) are prevalent in different systems and hold immense importance for maintaining/performing selective functions. The present study investigates the altered electrophysiological characteristics of the USM cell because of induction of Tamsulosin doses. Methods: The USM cell is described as an equivalent electrical circuit with several variable conductances representing two voltage-gated Ca2+ (T - type and L- type) channels, one voltage-gated fast potassium (KA) channel, one calcium-dependent large conductance potassium channel, and an HCN channel. A Tamsulosin drug model for the KA channel is simulated by multiplying the maximal conductance of the KA channel with a scaling factor between 0 and 1 to mimic the drug concentration. Results: The holding potential is fixed at ─ 75 mV for the voltage clamp protocol. Then the voltage steps up from ─ 80 mV to ─ 10 mV with a 10 mV step. In Fig 1, the red and blue solid lines represent simulated KA current under control and Tamsulosin dose. Fig 1 reveals that the KA current is elevated after the application of the Tamsulosin drug. As a result, the total outward current was reduced and the USM action potential duration was altered. It is also observed that the steady-state activation curve of the KA channel was shifted to more negative after applying Tamsulosin. Conclusions: This first in-silico study reveals the KA ionic current, which plays a major role in coordinating ureteral contractions, is altered due to Tamsulosin. It implicates that pharmacological maneuver of Tamsulosin is substantially beneficial for treating dysfunctional peristalsis to reduce symptoms from the ureteral stents procedure.