Effects of flufenamic acid in vivo on mmc activity and in vitro on intracellular calcium in the canine lower small intestine

Nitecki, S.; Farrugia, Gianrico; Rich, A M; Szurszewski, Joseph H.

doi:10.1016/0016-5085(94)90302-6

Cited by 4 publications

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“…NFA also produced an increase in [Ca 2 þ ] i in mesenteric artery smooth muscle cells, suggesting that the effect is not unique to pulmonary vascular smooth muscle cells. Increases in basal [Ca 2 þ ] i have previously been observed with both NFA and flufenamic acid in visceral smooth muscle cells (Nitecki et al, 1994), ST 885 cells (Poronnik et al, 1992), epithelial cells (Schultheiss et al, 2000), and neurones (Shaw et al, 1995;Partridge & Valenzuela, 2000).…”

Section: Discussionmentioning

confidence: 56%

“…Specifically, in bilayer studies, DIDS and 4-acetoamido-4 0 -isothiocyanatostilbene-2,2 0 -disulfonic acid (SITS) have been shown to activate the skeletal muscle ryanodine receptor, and lock it in an open state without decreasing the single-channel conductance (Kawasaki & Kasai, 1989). NFA was found to have a dual effect on the skeletal muscle ryanodine receptor, increasing the open probability of the channel at 10 mM and blocking the channel at 100 mM (Oba et al, 1996). A recent study on cardiac ryanodine receptors has shown that DIDS increased single-channel conductance and open probability, and altered the voltage dependence of channel gating (Hill & Sitsapesan, 2002).…”

Section: Discussionmentioning

confidence: 99%

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The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells

Cruickshank

Baxter

Drummond

2003

British J Pharmacology

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1 The effect of the Cl À channel blockers niflumic acid (NFA), 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4 0 -diisothiocyanatostilbene-2,2 0 -disulfonic acid (DIDS), and anthracene-9-carboxylic acid (A-9-C), on Ca 2 þ signalling in rat pulmonary artery smooth muscle cells was examined. Intracellular Ca 2 þ concentration ([Ca 2 þ ] i ) was monitored with either fura-2 or fluo-4, and caffeine was used to activate the ryanodine receptor, thereby releasing Ca 2 þ from the sarcoplasmic reticulum (SR). 2 NFA and NPPB significantly increased basal [Ca 2 þ ] i and attenuated the caffeine-induced increase in [Ca 2 þ ] i . These Cl À channel blockers also increased the half-time (t 1/2 ) to peak for the caffeineinduced [Ca 2 þ ] i transient, and slowed the removal of Ca 2 þ from the cytosol following application of caffeine. Since DIDS and A-9-C were found to adversely affect fura-2 fluorescence, fluo-4 was used to monitor intracellular Ca 2 þ in studies involving these Cl À channel blockers. Both DIDS and A-9-C increased basal fluo-4 fluorescence, indicating an increase in intracellular Ca 2 þ , and while DIDS had no significant effect on the t 1/2 to peak for the caffeine-induced Ca 2 þ transient, it was significantly increased by A-9-C. 3 In the absence of extracellular Ca 2 þ , NFA significantly increased basal [Ca 2 þ ] i , suggesting that the release of Ca 2 þ from an intracellular store was responsible for the observed effect. 4 Depleting the SR with the combination of caffeine and cyclopiazonic acid prevented the increase in basal [Ca 2 þ ] i induced by NFA. Additionally, incubating the cells with ryanodine also prevented the increase in basal [Ca 2 þ ] i induced by NFA. 5 These data show that Cl À channel blockers have marked effects on Ca 2 þ signalling in pulmonary artery smooth muscle cells. Furthermore, examination of the NFA-induced increase in [Ca 2 þ ] i indicates that it is likely due to Ca 2 þ release from an intracellular store, most probably the SR.

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Section: Discussionmentioning

confidence: 56%

Section: Discussionmentioning

confidence: 99%

The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells

Cruickshank

Baxter

Drummond

2003

British J Pharmacology

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“…10Fenamates have also been found to inhibit calcium activated chloride channels in Xenopus oocytes11 and to activate large conductance calcium activated potassium channels 1213 and in human and canine jejunal circular smooth muscle cells, fenamates have two separate effects, one on outward potassium current and the membrane potential14 15 and the other on intracellular calcium 16. Flufenamic acid markedly increases outward potassium currents and hyperpolarises the membrane potential.…”

mentioning

confidence: 99%

“…The second cellular effect of flufenamic acid is on intracellular calcium. Flufenamic acid markedly increases intracellular calcium when applied at the dose of 500 μM 16. An increase in intracellular calcium would be expected to cause smooth muscle contraction.…”

mentioning

confidence: 99%

The effect of flufenamic acid on gastrointestinal myoelectrical activity and transit time in dogs

Farrugia

Nitecki

Harty

et al. 1998

Gut

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Block of hippocampal CAN channels by flufenamate

Partridge

Valenzuela

2000

Brain Research

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Effects of flufenamic acid in vivo on mmc activity and in vitro on intracellular calcium in the canine lower small intestine

Cited by 4 publications

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The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells

The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells

The effect of flufenamic acid on gastrointestinal myoelectrical activity and transit time in dogs

Block of hippocampal CAN channels by flufenamate

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Effects of flufenamic acid in vivo on mmc activity and in vitro on intracellular calcium in the canine lower small intestine

Cited by 4 publications

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The Cl− channel blocker niflumic acid releases Ca2+ from an intracellular store in rat pulmonary artery smooth muscle cells

The Cl− channel blocker niflumic acid releases Ca2+ from an intracellular store in rat pulmonary artery smooth muscle cells

The effect of flufenamic acid on gastrointestinal myoelectrical activity and transit time in dogs

Block of hippocampal CAN channels by flufenamate

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The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells

The Cl⁻ channel blocker niflumic acid releases Ca²⁺ from an intracellular store in rat pulmonary artery smooth muscle cells