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Abstract

Hypercholesterolemia (HC) is associated with impaired endothelium-dependent vasodilation, while statins improve endothelial function. An apparently “paradoxical” increase of nitrogen oxydes release by endothelium is also reported in early stages of experimental HC. Aim of the study was to assess systemic Nitric Oxyde (NO) generation and endothelium dependent and independent vasodilation in young subjects with early familial HC (FHC) and no cardiovascular disease, before and 3 months after Atorvastatin therapy, 10 mg/day. Methods: in 12 FHC subjects (age 28±2 years, total cholesterol 291±22 mg) and 12 healthy controls (26±3 years) brachial artery diameter was measured by ultrasound at rest, after 5 min forearm ischemia (flow-mediated dilation, FMD) and after sublingual glyceryl trinitrate (GTN 400 mg). Plasma nitrates and nitrites (NOx) were measured as markers of NO release by a colorimetric assay (Griess reaction).

Results are in Table:

ControlsFHC Before TherapyFHC After Therapy
TC (mg%) )170±28291±22211±31*^
NOx (mmol)35±2587±10*63±10
CSA (mm2)22.5±3.09.6±3.8*9.7±2.4*
FMD (%)14±621±13*32±11*^
GTN (%)46±343±0.445±1.6
ControlsFHC Before TherapyFHC After Therapy
TC (mg%) )170±28291±22211±31*^
NOx (mmol)35±2587±10*63±10
CSA (mm2)22.5±3.09.6±3.8*9.7±2.4*
FMD (%)14±621±13*32±11*^
GTN (%)46±343±0.445±1.6
ControlsFHC Before TherapyFHC After Therapy
TC (mg%) )170±28291±22211±31*^
NOx (mmol)35±2587±10*63±10
CSA (mm2)22.5±3.09.6±3.8*9.7±2.4*
FMD (%)14±621±13*32±11*^
GTN (%)46±343±0.445±1.6
ControlsFHC Before TherapyFHC After Therapy
TC (mg%) )170±28291±22211±31*^
NOx (mmol)35±2587±10*63±10
CSA (mm2)22.5±3.09.6±3.8*9.7±2.4*
FMD (%)14±621±13*32±11*^
GTN (%)46±343±0.445±1.6

(* p<0.05 vs control; ^ p<0.05 after therapy vs before therapy)

Plasma NOx were significantly higher in FHC than in controls before treatment and decreased after Atorvastatin. In FHC, basal cross sectional vessel area (CSA) was lower than in controls before therapy, resulting in higher percent of increase during reactive hyperemia. After therapy, an additional increase in FMD was obtained with similar basal CSA of brachial artery. Dilatation in response to GTN was comparable in all groups. Conclusion: in early FHC, the finding of increased plasma NOx, reduced baseline arterial size, and preserved FMD suggest the coexistence of endothelial “activation” with increased release of NO, reduced NO “tonic” bioavailability and preserved stimulated NO activity. Atorvastatin seems to reduce endothelial activation and to improve FMD.

Nitric Oxide, Hypercholesterolemia, Vasodilation
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© American Journal of Hypertension, Ltd. 2001
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