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Mesenteric Resistance Arteries (mesenteric + resistance_artery)

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Medical Sciences	100%

Selected Abstracts

Reactive Oxygen Species Are Necessary for High Flow (Shear Stress)-induced Diameter Enlargement of Rat Resistance Arteries

MICROCIRCULATION, Issue 5 2009
ERIC J. BELIN DE CHANTEMÈLE
ABSTRACT Objectives: Chronic increases in blood flow induce remodeling associated with increases in diameter and endothelium-mediated dilation. Remodeling requires cell growth and migration, which may involve reactive oxygen species (ROS). Nevertheless, the role of ROS in flow-mediated remodeling in resistance arteries is not known. Materials and Methods: Rat mesenteric resistance arteries (MRAs) were exposed to high flow (HF) by sequentially ligating second-order MRAs in vivo. After three weeks, arteries were collected for structural, pharmacological, and biochemical analysis. Results: In HF arteries, luminal diameter (431±12 to 553±14 ,m; n=10), endothelium (acetylcholine)-mediated vasodilatation (61±6 to 77±6% relaxation) and NAD(P)H subunit (gp91phox and p67phox) expression levels, and ROS (dihydroethydine microphotography) and peroxynitrite (3-nitro-tyrosine) production were higher than in normal flow arteries. Acute ROS scavenging with tempol improved acetylcholine-dependent relaxation (92±4% relaxation), confirming that ROS are produced in HF arteries. Chronic treatment with tempol prevented the increase in diameter, reduced ROS and peroxynitrite production, and improved endothelium-mediated relaxation in HF arteries. Thus, ROS and NO were involved in HF-induced diameter enlargement, possibly through the formation of peroxynitrite, while ROS reduced the increase in endothelium-dependent relaxation. Conclusions: ROS production is necessary for flow-mediated diameter enlargement of resistance arteries. However, ROS counteract, in part, the associated improvement in endothelium-mediated relaxation. [source]

Involvement of H2O2 in superoxide-dismutase-induced enhancement of endothelium-dependent relaxation in rabbit mesenteric resistance artery

BRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2003
Takeo Itoh
The mechanism underlying the enhancement by superoxide dismutase (SOD) of endothelium-dependent relaxation was investigated in rabbit mesenteric resistance arteries. SOD (200 U ml,1) increased the production of H2O2 in smooth muscle cells (as indicated by the use of an H2O2 -sensitive fluorescent dye). Neither SOD nor catalase (400 U ml,1) modified either the resting membrane potential or the hyperpolarization induced by acetylcholine (ACh, 1 ,M) in smooth muscle cells. In arteries constricted with noradrenaline, the endothelium-dependent relaxation induced by ACh (0.01,1 ,M) was enhanced by SOD (200 U ml,1) (P<0.01). This action of SOD was inhibited by L - NG -nitroarginine (nitric oxide (NO)-synthase inhibitor) but not by either charybdotoxin+apamin (Ca2+ -activated-K+ -channel blockers) or diclofenac (cyclooxygenase inhibitor). Neither ascorbate (50 ,M) nor tiron (0.3 mM), superoxide scavengers, had any effect on the ACh-induced relaxation, but each attenuated the enhancing effect of SOD on the ACh-induced relaxation. Similarly, catalase (400 U ml,1) inhibited the effect of SOD without changing the ACh-induced relaxation. In endothelium-denuded strips constricted with noradrenaline, SOD enhanced the relaxation induced by the NO donor 1-hydroxy-2-oxo-3-(N -methyl-3-aminopropyl)-3-methyl-1-triazene (NOC-7) (P<0.05). Ascorbate and catalase each attenuated this effect of SOD. H2O2 (1 ,M) enhanced the relaxation on the noradrenaline contraction induced by NOC-7 and that induced by 8-bromo-cGMP, a membrane-permeable analogue of guanosine 3,,5, cyclic monophosphate (cGMP). SOD had no effect on cGMP production, whether measured in endothelium-intact strips following an application of ACh (0.1 ,M) or in endothelium-denuded strips following an application of NOC-7 (0.1 ,M). It is suggested that in rabbit mesenteric resistance arteries, SOD increases the ACh-induced, endothelium-dependent relaxation by enhancing the action of NO in the smooth muscle via its H2O2 -producing action (rather than via a superoxide-scavenging action). British Journal of Pharmacology (2003) 139, 444,456. doi:10.1038/sj.bjp.0705255 [source]

Fluvastatin remodels resistance arteries in genetically hypertensive rats, even in the absence of any effect on blood pressure

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2002
Janet M Ledingham
Summary 1.,The aims of the present study were, first, to determine whether, in the genetically hypertensive (GH) rat, fluvastatin would lower blood pressure and remodel mesenteric resistance arteries (MRA) and the basilar artery and, second, to see whether treatment with a combination of fluvastatin and the angiotensin receptor antagonist valsartan would have any extra beneficial effect on blood pressure and vascular remodelling. 2.,Male GH rats had tail-cuff systolic blood pressure (SBP) monitored weekly from the age of 7 to 12 weeks. Groups (n = 12,14) were treated with fluvastatin (4 mg/kg per day), valsartan (5 mg/kg per day), both mixed in with chow, or a combination of fluvastatin 4 mg/kg per day + valsartan 5 mg/kg per day. Untreated GH and a group of normotensive Wistar (N) rats served as control groups. 3.,At 12 weeks of age, intra-arterial (i.a.) blood pressure was measured by femoral cannulation and rats were then perfused (at the SBP of the animal) with Tyrode's solution containing heparin and papaverine followed by 2.5% glutaraldehyde in Tyrode's solution; MRA and basilar arteries were embedded in Technovit. Serial sections were cut and Giemsa stained and stereological methods used to obtain media width, lumen diameter, medial cross-sectional area (CSA) and the ratio of media width to lumen diameter. Hearts were weighed to determine left ventricular (LV) mass. 4.,Fluvastatin had no effect on blood pressure or LV mass, whereas valsartan given alone or with fluvastatin significantly reduced both parameters. 5.,In MRA, fluvastatin reduced medial CSA, increased lumen size and, therefore, probably decreased vascular resistance. The media/lumen ratio was reduced to a level below that seen with the combination treatment and to below that of the N group. 6.,In the basilar artery, fluvastatin and valsartan showed similar outward remodelling of the lumen and reduction in the media/lumen ratio. The combination treatment group showed, in addition, a reduction in medial CSA and an even lower ratio than the GH group on fluvastatin or valsartan alone or the N group. 7.,Although fluvastatin has no effect on blood pressure, it does cause significant remodelling of MRA and the basilar artery. These beneficial structural changes in a peripheral resistance artery bed and in an artery involved in regulating resistance in the brain are worthy of further study. [source]

Effects Of Nitric Oxide Synthase Inhibition And Low-Salt Diet On Blood Pressure And Mesenteric Resistance Artery Remodelling In Genetically Hypertensive Rats

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2001
Janet M Ledingham
SUMMARY 1. Nitric oxide synthase (NOS)-inhibited genetically hypertensive (GH) rats on normal and low-sodium diets were additionally given valsartan or felodipine to establish whether low-Na intake would have extra beneficial effects on blood pressure and cardiovascular structure. 2. Male GH rats on normal or low-Na diets were treated with the NOS inhibitor NG -nitro- L -arginine methyl ester (L -NAME) from the age of 7 to 12 weeks and were given either valsartan (10 mg/kg per day) or felodipine (30 mg/kg per day). 3. Systolic blood pressure (SBP; tail-cuff) was measured weekly. At 12 weeks of age, mesenteric resistance arteries (MRA) were fixed by perfusion and embedded in Technovit (Heraeus Kulzer GmbH, Werheim, Germany). Serial sections were cut and stained. Stereological analysis was used to obtain MRA media width, lumen diameter, ratio of media width/lumen diameter (M/L) and medial cross-sectional area (CSA). Left ventricular (LV) mass was determined. 4. In GH L -NAME-treated rats on a normal diet, SBP was significantly reduced (P < 0.001) by valsartan and felodipine, as was LV mass (valsartan P < 0.001; felodipine P < 0.05). A low-Na diet with valsartan caused a further fall in SBP (P < 0.01) but, with felodipine, SBP increased in rats on a low-Na diet (P < 0.05). 5. Valsartan with the low-Na diet had no further effect on LV mass, but the felodipine-treated group on a low-Na diet had a lower LV mass (P < 0.05) than rats on a normal diet. 6. In MRA from the GH L -NAME + valsartan-treated group, there was hypotrophic inward remodelling; the M/L ratio was reduced (P < 0.001) compared with GH L -NAME-treated rats. The lumen was outwardly remodelled in the group on the low-Na diet. 7. The GH L -NAME + felodipine-treated group showed hypotrophic outward remodelling and a reduction in M/L ratio compared with the GH L -NAME-treated group (P < 0.001). A low-Na diet had no further effect on MRA. 8. A low-Na diet + valsartan had beneficial effects on SBP and MRA, where outward remodelling of the lumen occurred and, thus, resistance was reduced. In contrast, felodipine with a low-Na diet increased SBP, reduced LV mass and had no effect on MRA structure. Valsartan treatment with a low-Na diet confers extra benefits on blood pressure and MRA structure. [source]