Document Detail


Mechanism of lipid enhancement of alpha1-adrenoceptor pressor sensitivity in hypertension.
MedLine Citation:
PMID:  16794488     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE AND DESIGN: Plasma lipids enhance alpha1-adrenoceptor pressor sensitivity, impair baroreflex function, and correlate with increased blood pressure. This clinical study was designed to determine whether the enhanced alpha1-pressor sensitivity induced by acute hyperlipidemia is primarily mediated by increased vascular alpha1 responsiveness, reduced baroreflex sensitivity (BRS) or both. METHOD: Regional alpha1-adrenoceptor vasoreactivity was measured using a graded brachial artery infusion of the alpha1 agonist, phenylephrine, in seven subjects with stage 1 hypertension. Forearm blood flow was estimated from venous occlusion plethysmography. The phenylephrine dose-forearm blood flow response curve was used to determine alpha1-vascular reactivity (slope of the dose-response curve) and sensitivity, EC50 (phenylephrine dose inducing 50% maximal response). BRS (ms/mmHg) was measured as the slope of the progressive rise in systolic blood pressure and the resultant lengthening in the subsequent R-R interval after systemic intravenous boluses of phenylephrine. Subsequently, plasma lipids were raised with a 1-h systemic co-infusion of intralipid and heparin, after which measurements of regional vasoreactivity and BRS were repeated. RESULTS: Mean arterial pressure was 109 +/- 4 versus 110 +/- 3 (P = NS), vasoreactivity was -0.71 +/- 0.10 versus -0.82 +/- 0.10 (P = NS) and log EC50 was 1.47 +/- 0.29 versus 1.52 +/- 0.34 nmol/l (P = NS) before and after raising non-esterified fatty acids, respectively. In contrast, mean BRS was acutely reduced from 8.2 +/- 2.1 to 6.2 +/- 1.8 ms/mmHg (P = 0.02) after the lipid infusion. CONCLUSIONS: These findings suggest that in hypertensive patients, the primary mechanism for short-term alpha1-pressor hypersensitivity in response to hyperlipidemia is via the acute impairment of BRS.
Authors:
Crystal A Gadegbeku; M Zakarea Shrayyef; Timothy P Taylor; Brent M Egan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Journal of hypertension     Volume:  24     ISSN:  0263-6352     ISO Abbreviation:  J. Hypertens.     Publication Date:  2006 Jul 
Date Detail:
Created Date:  2006-06-23     Completed Date:  2006-10-19     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  1383-9     Citation Subset:  IM    
Affiliation:
Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109-0725, USA. cgadegbe@umich.edu
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MeSH Terms
Descriptor/Qualifier:
Adrenergic alpha-Agonists / pharmacology
Baroreflex / drug effects,  physiology*
Blood Pressure / drug effects,  physiology*
Fatty Acids, Nonesterified / blood
Female
Humans
Hyperlipidemias / chemically induced,  physiopathology*
Hypertension / blood,  physiopathology*
Male
Middle Aged
Phenylephrine / pharmacology
Receptors, Adrenergic, alpha-1 / physiology*
Triglycerides / blood
Vascular Resistance / drug effects,  physiology
Grant Support
ID/Acronym/Agency:
K23 RR15542/RR/NCRR NIH HHS; K24 HL04290/HL/NHLBI NIH HHS; M01 RR00042/RR/NCRR NIH HHS; M01 RR01070/RR/NCRR NIH HHS; R01 58794//PHS HHS
Chemical
Reg. No./Substance:
0/Adrenergic alpha-Agonists; 0/Fatty Acids, Nonesterified; 0/Receptors, Adrenergic, alpha-1; 0/Triglycerides; 59-42-7/Phenylephrine

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


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