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  • Title: [Ionic perturbations produced by a non-laminar flow in vascular smooth muscle cells in culture. Protection by cicletanine via a cyclo-oxygenase metabolite].
    Author: Rosati C, Cavalier S, Braquet P, Berthet P, Tarrade T, Ruchoux MM, Garay R.
    Journal: Arch Mal Coeur Vaiss; 1989 Nov; 82 Spec No 4():41-4. PubMed ID: 2514667.
    Abstract:
    The non-laminar (rather turbulent) flow, induced by cell washings was able to reversibly increase internal Na+ contents in cultured aortic smooth muscle (A10 cells). Similar changes (although to a lesser extent) were observed in cardiocytes but not in fibroblasts, erythrocytes, thymocytes or macrophages, suggesting that they are specific for excitable cells. The increased vascular sodium content had the following properties: it was inhibited by nitrendipine; it was accompanied by an increase in free cytosolic Ca2 contents; it was unable to stimulate the sodium pump and (iv) it reflected the qualitative and quantitative composition of the incubation media. These observations suggested to us that the increased vascular sodium content results from the opening of potential-dependent calcium channels with secondary internalisation of high amounts of extracellular ions. The ionic perturbations were blocked by low concentrations of cicletanine (IC50 of about 10(-9) M on intracellular sodium). Moreover, the protective effects of cicletanine were inhibited by indomethacin, suggesting that they are mediated by a cyclo-oxygenase metabolite, perhaps prostacyclin. Sodium nitroprusside, a compound able to stimulate calcium entry in the sarcoplasmic reticulum via cyclic GMP, was also able to protect vascular cells (although it acted at higher concentrations than cicletanine). Conversely, captopril and diuretic drugs such as hydrochlorothiazide, furosemide, spironolactone and acetazolamide were unable to protect vascular cells against the deleterious effects of cell washings.
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