Malfunction in ion channels, due to mutations in genes encoding channel pro
teins or the presence of autoantibodies, are increasing being implicated in
causing disease conditions, termed channelopathies. Dysfunction of potassi
um (K+) channels has been associated with the pathophysiology of a number o
f neurological, as well as peripheral, disorders (e.g., episodic ataxia, ep
ilepsy, neuromyotonia, Parkinson's disease, congenital deafness, long QT sy
ndrome). K+ channels, which demonstrate a high degree of diversity and ubiq
uity, are fundamental in the control of membrane depolarisation and cell ex
citability. A common feature of K+ channelopathies is a reduction or loss o
f membrane potential repolarisation. The identification of K+ channel subty
pe specific openers will allow the recovery of the mechanism(s) responsible
for counteraction of uncontrolled cellular depolarisation. Synthetic agent
s that demonstrate K+ channel opening properties are available for a variet
y of K+ channel subtypes (e.g., K-ATP, BKCa, GIRK and M-channel). This stud
y reviews the realistic therapeutic potential that may be gained in a broad
spectrum of clinical conditions by K+ channel openers. K+ channel openers
would therefore identify dysfunctional K+ channel as therapeutic targets fo
r clinical benefit, in addition being able to modulate normally functioning
K+ channels to gain clinical management of pathophysiological events irres
pective of the cause.