Mössbauer and magnetic study of CoxFe3-xO4 nanoparticles

International audienceMagnetic nanoparticles of cobalt ferrites CoxFe3-xO4 (x=1 or 2) have been obtained either by mechanical milling or thermal treatment of pre-prepared layered double hydroxide carbonate x- LDH–CO3. Mechanical milling of the 1-LDH–CO3 leads to the large-scale preparation of nearly spherical nanoparticles of CoFe2O4, the size of which (5 to 20 nm) is controlled by the treatment time. Core-shell structure with surface spin-canting has been considered for the nanoparticles formed to explain the observed hysteresis loop shift (from ZFC–FC) in the magnetic properties. Annealing treatment of the 2-LDH–CO3 below 673 K results in the formation of nearly spherical pure Co2FeO4 nanoparticles. At 673 K and above, the LDH decomposition leads to the formation of a mixture of both spinels phases Co2FeO4 and CoFe2O4, the amount of the latter increases with annealing temperature. Unusually high magnetic hardness characterized by a 22 kOe coercive field at 1.8 K has been observed, which reflects the high intrinsic anisotropy for Co2FeO4. Key words CoxFe3-xO4 (x =1, 2) nanoparticles . ferrite spinel . high energy ball-milling . high coercivity . Mössbauer Nano-sized materials are currently of great technological importance and consequently, one of the research subjects under intense investigation for their mechanical, electrical or chemical properties due to the fact that the properties of the nanophases being very different from those of the bulk material. Nanoparticles of materials are likely to improve dramatically the properties of the resulting material. Consequently, the synthesis of spinel ferrite nanoparticles has been intensively studied in recent years due to their potential application in high-density magnetic recording, microwave devices and magnetic fluids

Chronic ethanol intake modulates vascular levels of endothelin-1 receptor and enhances the pressor response to endothelin-1 in anaesthetized rats

Background and purpose: The contribution of endothelin-1 (ET-1) to vascular hyper-reactivity associated with chronic ethanol intake, a major risk factor in several cardiovascular diseases, remains to be investigated. Experimental approach: The biphasic haemodynamic responses to ET-1 (0.01-0.1 nmol kg(-1), i.v.) or to the selective ET(B) agonist, IRL1620 (0.001-1.0 nmol kg(-1), i.v.), with or without ET(A) or ET(B) antagonists (BQ123 (c(DTrp-Dasp-Pro-Dval-Leu)) at 1 and 2.5 mg kg(-1) and BQ788 (N-cis-2,6-dimethyl-piperidinocarbonyl-L-gamma-methylleucyl1-D-1methoxycarbonyltryptophanyl-D-norleucine) at 0.25 mg kg(-1), respectively) were tested in anaesthetized rats, after 2 weeks` chronic ethanol treatment. Hepatic parameters and ET receptor protein levels were also determined. Key results: The initial hypotensive responses to ET-1 or IRL1620 were unaffected by chronic ethanol intake, whereas the subsequent pressor effects induced by ET-1, but not by IRL1620, were potentiated. BQ123 at 2.5 but not 1 mg kg(-1) reduced the pressor responses to ET-1 in ethanol-treated rats. Conversely, BQ788 (0.25 mg kg(-1)) potentiated ET-1-induced increases in mean arterial blood pressure in control as well as in ethanol-treated rats. Interestingly, in the latter group, increases in heart rate, induced by ET-1 at a dose of 0.025 mg kg(-1) were enhanced following ET(B) receptor blockade. Finally, we observed higher levels of ET(A) receptor in the heart and mesenteric artery and a reduction of ET(B) receptor protein levels in the aorta and kidney from rats chronically treated with ethanol. Conclusions and implications: Increased vascular reactivity to ET-1 and altered protein levels of ET(A) and ET(B) receptors could play a role in the pathogenesis of cardiovascular complications associated with chronic ethanol consumption

Functional characterization and expression of endothelin receptors in rat carotid artery: involvement of nitric oxide, a vasodilator prostanoid and the opening of K(+) channels in ET(B)-induced relaxation

1. We aimed to functionally characterize endothelin (ET) receptors in the rat carotid artery. mRNA and protein expressions of both ET(A) and ET(B) receptors, evaluated by reverse transcription–polymerase chain reaction (RT–PCR) and Western immunoblotting, were detected in carotid segments. Immunohistochemical assays showed that ET(B) receptors are expressed in the endothelium and smooth muscle cells, while ET(A) receptors are expressed only in the smooth muscle cells. In endothelium-denuded vessels, levels of ET(B) receptor mRNA were reduced. 2. Vascular reactivity experiments, using standard muscle bath procedures, showed that ET-1 induces contraction in endothelium-intact and -denuded carotid rings in a concentration-dependent manner. Endothelial removal enhanced ET-1-induced contraction. BQ123 and BQ788, selective antagonists for ET(A) and ET(B) receptors, respectively, produced concentration-dependent rightward displacements of the ET-1 concentration–response curves. 3. IRL1620, a selective agonist for ET(B) receptors, induced a slight vasoconstriction that was abolished by BQ788, but not affected by BQ123. IRL1620-induced contraction was augmented after endothelium removal. 4. ET-1 concentration dependently relaxed phenylephrine-precontracted rings with intact endothelium. The relaxation was augmented in the presence of BQ123, reduced in the presence of BQ788 and completely abolished after endothelium removal. IRL1620 induced vasorelaxation that was abolished by BQ788 and endothelium removal, but not affected by BQ123. 5. Preincubation of intact rings with N(G)-nitro-L-arginine methyl ester (L-NAME), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), indomethacin or tetraethylammonium (TEA) reduced IRL1620-induced relaxation. The combination of L-NAME, indomethacin and TEA completely abolished IRL1620-induced relaxation while sulfaphenazole did not affect this response. 4-aminopyridine (4-AP), but not apamin, glibenclamide or charybdotoxin, reduced IRL1620-induced relaxation. 6. The major finding of this work is that it firstly demonstrated functionally the existence of both ET(A) and ET(B) vasoconstrictor receptors located on the smooth muscle of rat carotid arteries and endothelial ET(B) receptors that mediated vasorelaxation via NO–cGMP pathway, vasodilator cyclooxygenase product(s) and the activation of voltage-dependent K(+) channels

Endothelial overexpression of endothelin-1 modulates aortic, carotid, iliac and renal arterial responses in obese mice

Endothelin-1 (ET-1) is essential for mammalian development and life, but it has also been implicated in increased cardiovascular risk under pathophysiological conditions. The aim of this study was to determine the impact of endothelial overexpression of the prepro-endothelin-1 gene on endothelium-dependent and endothelium-independent responses in the conduit and renal arteries of lean and obese mice. Obesity was induced by high-fat-diet (HFD) consumption in mice with Tie-1 promoter-driven, endothelium-specific overexpression of the prepro-endothelin-1 gene (TET(het)) and in wild-type (WT) littermates on a C57BL/6N background. Isometric tension was measured in rings (with endothelium) of the aorta (A), carotid (CA) and iliac (IA) arteries as well as the main (MRA) and segmental renal (SRA) arteries; all experiments were conducted in the absence or presence of L-NAME and/or the COX inhibitor meclofenamate. The release of prostacyclin and thromboxane A2 was measured by ELISA. In the MRA, TET(het) per se increased contractions to endothelin-1, but the response was decreased in SRA in response to serotonin; there were also improved relaxations to acetylcholine but not insulin in the SRA in the presence of L-NAME. HFD per se augmented the contractions to endothelin-1 (MRA) and to the thromboxane prostanoid (TP) receptor agonist U46619 (CA, MRA) as well as facilitated relaxations to isoproterenol (A). The combination of HFD and TET(het) overexpression increased the contractions of MRA and SRA to vasoconstrictors but not in the presence of meclofenamate; this combination also augmented further relaxations to isoproterenol in the A. Contractions to endothelin-1 in the IA were prevented by endothelin-A receptor antagonist BQ-123 but only attenuated in obese mice by BQ-788. The COX-1 inhibitor FR122047 abolished the contractions of CA to acetylcholine. The release of prostacyclin during the latter condition was augmented in samples from obese TET(het) mice and abolished by FR122047. These findings suggest that endothelial TET(het) overexpression in lean animals has minimal effects on vascular responsiveness. However, if comorbid with obesity, endothelin-1-modulated, prostanoid-mediated renal arterial dysfunction becomes apparent