Chronic pinacidil attenuates the pentylenetetrazole‑induced kindling in rats.

Seizures in epilepsy result from excessive neuronal electrical discharges. Imbalances in potassium homeostasis can increase neuronal excitability and trigger epileptic seizures. Drugs that enhance potassium currents are expected to suppress seizures. Pinacidil, an ATP‑sensitive potassium channel opener, has shown anticonvulsant effects in acute seizure models in rodents. However, its effects following chronic systemic administration in pentylenetetrazole (PTZ)-kindled rats remain unknown. The aim of this study was to investigate the impact of long‑term pinacidil treatment in the PTZ‑kindling model of epilepsy. Male Wistar Hannover rats were treated intraperitoneally with pinacidil 30 min before each PTZ injection, administered intraperitoneally every other day for 27 days (14 injections). Behavioral responses were recorded for 30 min immediately after each PTZ injection. Twenty‑four hours after the last PTZ injection, animals underwent the rotarod test and were then euthanized for toxicological analysis of renal and hepatic biochemical markers in serum. Chronic pinacidil treatment prevented the development of PTZ‑induced kindling. Biochemical data showed that chronic pinacidil did not provoke changes in serum creatinine and urea levels or in aspartate aminotransferase and alanine aminotransferase levels. These findings suggest that long‑term administration of pinacidil impairs the progression of PTZ‑induced kindling without causing nephrotoxic or hepatotoxic effects.