5,6-EET potently inhibits T-type calcium channels: implication in the regulation of the vascular tone

被引:0
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作者
Magali Cazade
Isabelle Bidaud
Pernille B. Hansen
Philippe Lory
Jean Chemin
机构
[1] Institut de Génomique Fonctionnelle,Centre National de la Recherche Scientifique (CNRS) Unité Mixte de Recherche (UMR) 5203
[2] Universités Montpellier 1 & 2,INSERM U661
[3] Institut de Génomique Fonctionnelle,LabEx ‘Ion Channel Science and Therapeutics’
[4] Universités Montpellier 1 & 2,Cardiovascular and Renal Research
[5] Institut de Génomique Fonctionnelle,undefined
[6] Universités Montpellier 1 & 2,undefined
[7] University of Southern Denmark,undefined
关键词
Ca; 3.2; 5,6-EET; Vasodilation; Mesenteric; Knockout; Hypertension;
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学科分类号
摘要
T-type calcium channels (T-channels) are important actors in neuronal pacemaking, in heart rhythm, and in the control of the vascular tone. T-channels are regulated by several endogenous lipids including the primary eicosanoid arachidonic acid (AA), which display an important role in vasodilation via its metabolism leading to prostanoids, leukotrienes, and epoxyeicosatrienoic acids (EETs). However, the effects of these latter molecules on T-currents have not been investigated. Here, we describe the effects of the major cyclooxygenase, lipoxygenase, and cytochrome P450 epoxygenase products on the three human recombinant T-channels (Cav3.1, Cav3.2, and Cav3.3), as compared to those of AA. We identified the P450 epoxygenase product, 5,6-EET, as a potent physiological inhibitor of Cav3 currents. The effects of 5,6-EET were observed at sub-micromolar concentrations (IC50 = 0.54 μM), occurred in the minute range, and were reversible. The 5,6-EET inhibited the Cav3 currents at physiological resting membrane potentials mostly by inducing a large negative shift in their steady-state inactivation properties. Using knockout mice for Cav3.1 and Cav3.2, we demonstrated that the vasodilation of preconstricted mesenteric arteries induced by 5,6-EET was specifically impaired in Cav3.2 knockout mice. Overall, our results indicate that inhibition of Cav3 currents by 5,6-EET is an important mechanism controlling the vascular tone.
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页码:1759 / 1768
页数:9
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