ArticleBritish journal of pharmacology1996
Effect of niflumic acid on noradrenaline-induced contractions of the rat aorta.
Article in British journal of pharmacology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 90 citations in OpenAlex.
- TMEM16A in gastrointestinal and vascular smooth muscle contractility.The Journal of physiology · 2025Review
- A small molecule inhibitor of the chloride channel TMEM16A blocks vascular smooth muscle contraction and lowers blood pressure in spontaneously hypertensive rats.Kidney international · 2021Article
- Calcium-Activated Chloride Channels in Myometrial and Vascular Smooth Muscle.Frontiers in physiology · 2021Review
- A paradoxical increase of force development in saphenous and tail arteries from heterozygous ANO1 knockout mice.Physiological reports · 2020Article
- Molecular and functional significance of Ca(2+)-activated Cl(-) channels in pulmonary arterial smooth muscle.Pulmonary circulation · 2015Review
- Inhibitory role of phosphatidylinositol 4,5-bisphosphate on TMEM16A-encoded calcium-activated chloride channels in rat pulmonary artery.British journal of pharmacology · 2014Article
- TMEM16A knockdown abrogates two different Ca(2+)-activated Cl (-) currents and contractility of smooth muscle in rat mesenteric small arteries.Pflugers Archiv : European journal of physiology · 2014Article
- Cl⁻ channels in smooth muscle cells.Pflugers Archiv : European journal of physiology · 2014Review
- Potent vasorelaxant activity of the TMEM16A inhibitor T16A(inh) -A01.British journal of pharmacology · 2013Article
- A Ca²⁺-dependent chloride current and Ca²⁺ influx via Ca(v)1.2 ion channels play major roles in P2Y receptor-mediated pulmonary vasoconstriction.British journal of pharmacology · 2012Article
- Inhibition of Ca2+-activated Cl- channels by gallotannins as a possible molecular basis for health benefits of red wine and green tea.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Phosphorylation alters the pharmacology of Ca(2+)-activated Cl channels in rabbit pulmonary arterial smooth muscle cells.British journal of pharmacology · 2009Article
- Mechanisms of U46619-induced contraction of rat pulmonary arteries in the presence and absence of the endothelium.British journal of pharmacology · 2009Article
- Ca2+-activated Cl- current in retinal arteriolar smooth muscle.Investigative ophthalmology & visual science · 2009Article
- Effects of calcium channel blockers on antidepressant action of Alprazolam and Imipramine.The Libyan journal of medicine · 2007Article
- Mechanisms of U46619- and 5-HT-induced contraction of bovine pulmonary arteries: role of chloride ions.British journal of pharmacology · 2007Article
- Na+ -K+ -2Cl- cotransporter is implicated in gender differences in the response of the rat aorta to phenylephrine.British journal of pharmacology · 2006Article
- Identification of an N-terminal amino acid of the CLC-3 chloride channel critical in phosphorylation-dependent activation of a CaMKII-activated chloride current.The Journal of physiology · 2004Article
- Effects of chloride substitution on electromechanical responses in the pulmonary artery of Dahl normotensive and hypertensive rats.British journal of pharmacology · 2004Article
- Effects of chloride channel blockers on hypotonicity-induced contractions of the rat trachea.British journal of pharmacology · 2004Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
1. The effects of niflumic acid, an inhibitor of calcium-activated chloride channels, were compared with the actions of the calcium channel antagonist nifedipine on noradrenaline-evoked contractions in isolated preparations of the rat aorta. 2. The cumulative concentration-effect curve to noradrenaline (NA) was depressed by both nifedipine and niflumic acid in a reversible and concentration-dependent manner. The degree of inhibition of the maximal contractile response to NA (1 microM) produced by 10 microM niflumic acid (38%) was similar to the effect of 1 microM nifedipine (39%). 3. Contractions to brief applications (30 s) of 1 microM NA were inhibited by 55% and 62% respectively by 10 microM niflumic acid and 1 microM nifedipine. 4. In the presence of 0.1 microM nifedipine, niflumic acid (10 microM) produced no further inhibition of the NA-evoked contractions. Thus, the actions of niflumic acid and nifedipine were not additive. 5. In Ca-free conditions the transient contraction induced by 1 microM NA was not inhibited by niflumic acid (10 microM) and therefore this agent does not reduce the amount of calcium released from the intracellular store or reduce the sensitivity of the contractile apparatus to calcium. 6. Niflumic acid 10 microM did not inhibit the contractions produced by KCl (up to 120 mM) which were totally blocked by nifedipine. Contractions induced by 25 mM KCl were completely inhibited by 1 microM levcromakalim but were unaffected by niflumic acid. 7. It was concluded that niflumic acid produces selective inhibition of a component of NA-evoked contraction which is probably mediated by voltage-gated calcium channels. These data are consistent with a model in which NA stimulates a calcium-activated chloride conductance which leads to the opening of voltage-gated calcium channels to produce contraction.
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