Document Detail


Acute elevation of plasma non-esterified fatty acids increases pulse wave velocity and induces peripheral vasodilation in humans in vivo.
MedLine Citation:
PMID:  17309447     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Plasma NEFA (non-esterified fatty acid) concentrations are elevated in patients with obesity. In the present study we first aimed to provide an integral haemodynamic profile of elevated plasma NEFAs by the simultaneous assessment of blood pressure, pulse wave velocity, FBF (forearm blood flow) and sympathetic nervous system activity during acute elevation of NEFAs. Secondly, we hypothesized that NEFA-induced vasodilation is mediated by adenosine receptor stimulation. In a randomized cross-over trial in healthy subjects, Intralipid was infused for 2 h to elevate plasma NEFAs. Glycerol was administered as the Control infusion. We assessed blood pressure, pulse wave velocity, FBF (using venous occlusion plethysmography) and sympathetic nervous system activity by measurement of noradrenaline and adrenaline. During the last 15 min of Intralipid/Control infusion, the adenosine receptor antagonist caffeine (90 microg x min(-1) x dl(-1)) was administered into the brachial artery of the non-dominant arm. Compared with Control infusion, Intralipid increased pulse wave velocity, SBP (systolic blood pressure) and pulse pressure, as well as FBF (from 1.8+/-0.2 to 2.7+/-0.6 and from 2.3+/-0.2 to 2.7+/-0.6 ml x min(-1) x dl(-1) for Intralipid compared with Control infusion; P<0.05, n=9). Although in a positive control study caffeine attenuated adenosine-induced forearm vasodilation (P<0.01, n=6), caffeine had no effect on Intralipid-induced vasodilation (P=0.5). In conclusion, elevation of plasma NEFA levels increased pulse wave velocity, SBP and pulse pressure. FBF was also increased, either by baroreflex-mediated inhibition of the sympathetic nervous system or by a direct vasodilating effect of NEFAs. As the adenosine receptor antagonist caffeine could not antagonize the vasodilator response, this response is not mediated by adenosine receptor stimulation.
Authors:
Niels P Riksen; Marlies Bosselaar; Stephan J L Bakker; Robert J Heine; Gerard A Rongen; Cees J Tack; Paul Smits
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Publication Detail:
Type:  Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  113     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2007 Jul 
Date Detail:
Created Date:  2007-05-31     Completed Date:  2007-06-27     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  33-40     Citation Subset:  IM    
Affiliation:
Department of Pharmacology-Toxicology, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. N.Riksen@aig.umcn.nl
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MeSH Terms
Descriptor/Qualifier:
Adenosine / pharmacology*
Autonomic Nervous System
Blood Flow Velocity / drug effects
Blood Pressure / drug effects
Caffeine / pharmacokinetics
Compliance
Cross-Over Studies
Fat Emulsions, Intravenous / pharmacology
Fatty Acids, Unsaturated / metabolism*
Forearm / blood supply*
Humans
Insulin / blood
Pulse
Receptors, Purinergic P1 / drug effects
Vasodilation / drug effects
Vasodilator Agents / pharmacology*
Chemical
Reg. No./Substance:
0/Fat Emulsions, Intravenous; 0/Fatty Acids, Unsaturated; 0/Receptors, Purinergic P1; 0/Vasodilator Agents; 11061-68-0/Insulin; 58-08-2/Caffeine; 58-61-7/Adenosine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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