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Investigation of the differential effects of niflumic acid on Cl currents in vascular myocytes
Author(s) -
Greenwood Iain,
Leblanc Norm,
Sones William
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a521-c
Subject(s) - niflumic acid , washout , chemistry , myocyte , chloride channel , biophysics , patch clamp , medicine , electrophysiology , calcium , endocrinology , pharmacology , biochemistry , biology , organic chemistry
Previous studies showed that niflumic acid (NFA), an agent considered to be an effective inhibitor of calcium‐activated chloride currents (IClCa), also stimulates the channel when it is persistently activated (Piper et al ., J Physiol , 539 , –131, 2002). This effect is manifest in rabbit pulmonary artery myocytes as an increase in currents at all negative potentials co‐incident with an inhibition of outward currents, which is followed by a marked enhancement at all potentials upon washout of NFA. We have investigated whether these phenomena exist in other vascular myocytes. In mouse portal vein myocytes 100 μM NFA produced very little inhibition of outward IClCa but enhanced the holding current at −60 mV. No further increase in current was seen upon washout, In murine aortic myocytes NFA (10 μM and 100 μM) produced a transient inhibition of IClCa at all potentials followed by a small enhancement of currents at negative potentials. No further increase was observed upon washout. In contrast the stimulatory effects of NS1619 (30 μM) were similar in all three cell types. These data reflect the complex nature of calcium‐activated chloride channels in smooth muscle cells. This work was supported by the British Heart Foundation.