There are reports indicating that
diuretics including
chlorothiazide,
furosemide,
ethacrynic acid,
amiloride and
bumetanide can have
anticonvulsant properties. Intracellular acidification appears to be a mechanism for the
anticonvulsant action of some
diuretics. This study was conducted to investigate whether or not
triamterene, a K(+)-sparing
diuretic, can generate protection against
seizures induced by intravenous or intraperitoneal
pentylenetetrazole (PTZ) models. And to see if,
triamterene can withstand maximal electroshock seizure (MES) in mice. We also investigated to see if there is any connection between
triamterene's anti-seizure effect and
ATP-sensitive K(+) (
KATP) channels. Five days
triamterene oral administration (10, 20 and 40 mg/kg), significantly increased clonic seizure threshold which was induced by intravenous
pentylenetetrazole.
Triamterene (10, 20 and 40 mg/kg) treatment also increased the latency of clonic seizure and decreased its frequency in intraperitoneal PTZ model. Administration of
triamterene (20 mg/kg) also decreased the incidence of tonic seizure in MES-induced seizure. Co-administration of a KATP sensitive channel blocker,
glibenclamide, in the 6th day, 60 min before intravenous PTZ blocked
triamterene's
anticonvulsant effect. A KATP sensitive channel opener,
diazoxide, enhanced
triamterene's anti-seizure effect in both intravenous PTZ or MES seizure models. At the end,
triamterene exerts
anticonvulsant effect in 3 seizure models of mice including intravenous PTZ, intraperitoneal PTZ and MES. The anti-seizure effect of
triamterene probably is induced through
KATP channels.