Document Detail

Metabolic vasodilation in the human forearm is preserved in hypercholesterolemia despite impairment of endothelium-dependent and independent vasodilation.
MedLine Citation:
PMID:  10690343     Owner:  NLM     Status:  MEDLINE    
OBJECTIVE: Hypercholesterolemia has been shown to impair endothelium-mediated, nitric oxide (NO)-dependent responses to acetylcholine (ACh), serotonin, substance P and flow-mediated dilation. We have recently shown that NO contributes to metabolic vasodilation in the human forearm. We sought to determine whether metabolic vasodilation is impaired in healthy subjects with hypercholesterolemia. METHODS: We compared the forearm blood flow (FBF) responses to isotonic exercise, ACh and the endothelium-independent vasodilator sodium nitroprusside in young, otherwise healthy volunteers with hypercholesterolemia and controls before and after the NO inhibitor NG-monomethyl-L-arginine (L-NMMA). FBF was measured using venous occlusion plethysmography. Hypercholesterolemic (n = 20) and control (n = 20) subjects were age- and gender-matched. RESULTS: Total cholesterol (6.9 +/- 0.3 vs. 4.6 +/- 0.1 mmol/l, P < 0.0001), low density lipoprotein (4.9 +/- 0.4 vs. 2.7 +/- 0.1 mmol/l, P < 0.001) and triglyceride (1.3 +/- 0.2 vs. 0.8 +/- 0.1 mmol/l, P = 0.005) levels were higher in the hypercholesterolemic group. Basal FBF and resistance were similar in the two groups. Hypercholesterolemia impaired the peak FBF response to ACh (11.1 +/- 1.9 vs. 17.6 +/- 2.2 ml/100 ml/min, P = 0.03), and reduced the peak response to sodium nitroprusside (6.0 +/- 0.4 vs. 8.1 +/- 0.6 ml/100 ml/min, P < 0.01). However, hypercholesterolemia did not affect peak hyperemic FBF (13.1 +/- 1.0 vs. 13.2 +/- 1.0 ml/100 ml/min, P = 1.0) or the FBF volume repayment during the 1 or 5 min after exercise. Resting FBF was reduced by L-NMMA to a similar degree (by 33% vs. 40%, P = 0.17) in both groups. Although L-NMMA reduced peak hyperemic FBF (by 16% vs. 17%, P = 0.93) and the volume repaid after exercise in both groups, there were no differences between the two groups. CONCLUSIONS: Exercise-induced metabolic vasodilation is in part dependent on NO release. Hypercholesterolemia impairs NO-mediated vasodilation, but is not associated with a reduction in exercise-induced hyperemia. This may indicate that multiple compensatory mechanisms are operative in skeletal muscle metabolic vasodilation.
S J Duffy; G New; R W Harper; I T Meredith
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Cardiovascular research     Volume:  43     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  1999 Aug 
Date Detail:
Created Date:  2000-03-10     Completed Date:  2000-03-10     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  721-30     Citation Subset:  IM    
Cardiovascular Centre, Monash Medical Centre, Clayton, Melbourne, Australia.
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MeSH Terms
Acetylcholine / diagnostic use
Case-Control Studies
Endothelium, Vascular / drug effects,  metabolism*,  physiopathology
Enzyme Inhibitors / diagnostic use
Forearm / blood supply*
Hypercholesterolemia / metabolism*,  physiopathology*
Nitric Oxide / metabolism*
Nitric Oxide Synthase / antagonists & inhibitors
Nitroprusside / diagnostic use
Regional Blood Flow / drug effects
Vasodilator Agents / diagnostic use
omega-N-Methylarginine / diagnostic use
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 17035-90-4/omega-N-Methylarginine; 51-84-3/Acetylcholine; EC Oxide Synthase

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