In:
British Journal of Pharmacology, Wiley, Vol. 114, No. 6 ( 1995-03), p. 1222-1226
Abstract:
1 The antiarrythmic drug, clofilium, has been shown to block several types of K + channel currents. To investigate the effects of clofilium on the transient outward K + current ( I to ), a cloned I to ‐type cardiac K + channel (RHK1) was expressed in Xenopus oocytes and the drug effects were examined on whole cell currents. 2 Extracellular application of clofilium slightly inhibited the current at + 60 mV from a holding potential of −80 mV. However, it unexpectedly enhanced the current from a holding potential of −60 mV in a dose‐dependent manner (219 ± 39% of control at 100 μ m ). 3 This enhancement is probably due to an increase in the ratio of channels in the resting state during steady depolarization, since clofilium shifted the inactivation curve in the depolarizing direction. 4 LY97119, a tertiary ammonium analogue of clofilium, did not exhibit this enhancing effect but only inhibited the current. 5 Clofilium may be useful for the study of channel inactivation because this type of phenomenon has not been reported for any other drug.
Type of Medium:
Online Resource
ISSN:
0007-1188
,
1476-5381
DOI:
10.1111/bph.1995.114.issue-6
DOI:
10.1111/j.1476-5381.1995.tb13336.x
Language:
English
Publisher:
Wiley
Publication Date:
1995
detail.hit.zdb_id:
2029728-2
SSG:
15,3
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