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|Title:||Simvastatin improves cardiovascular sympathetic modulation and endothelial function of resistance arteries from hypercholesterolemic mice|
|Authors:||MORAES-SILVA, Ivana C.; SOUZA, L. E.; ROSSONI, L. V.; IRIGOYEN, M. C.|
|Citation:||FASEB JOURNAL, v.26, 2012|
|Abstract:||Can simvastatin treatment (S) alter sympathetic cardiovascular control and mesenteric resistance arteries (MRA) relaxation of LDL receptor knock out (L) mice? Male L mice were treated with S (2 mg/kg, i.p., 7 days) or vehicle. C67Bl/6 mice were used as control (C). Total cholesterol (TC), blood pressure (BP) and autonomic modulation were analyzed. MRA rings were studied in an isometric myograph. Concentration-response curves to Ach (0.01nM-30μM) were obtained in rings incubated for 30 min with L-NAME (100 μM), a NOS inhibitor, tetraethylammonium (TEA; 5mM), a K+ channel blocker, or with vehicle. TC was 3x higher and BP was increased (systolic:30%, diastolic:7%) in L vs. C whereas S had no effect. Cardiac autonomic balance, which was 3x higher, and sympathetic modulation to the vessels, 5x higher in L vs. C, were significantly reduced in L+S (17 and 57%, respectively). MRA % of relaxation to Ach was impaired in L (37±2%) vs. C (92±5%) while S restored it to 70±6%. In C MRA, L-NAME and TEA inhibited Ach-induced relaxation in 46±8% and 74±5%, respectively (p<0.05 L-NAME vs. TEA). This inhibition was ~90±2% in L for both drugs (p<0.05 vs. C); while S shifted it to 70±7% of relaxation inhibition (p<0.05 vs. C and L). S partially restored MRA endothelial function in L mainly by modulating NO concomitantly with an improved autonomic cardiovascular control even without changes in systemic BP and lipid levels.|
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Comunicações em Eventos - HC/InCor
Comunicações em Eventos - LIM/59
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