Document Detail


Increased coronary vascular resistance cannot be reduced by inhibiting sympathetic overactivity in hypertension.
MedLine Citation:
PMID:  12297708     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The aim of this study was to test whether increased coronary vascular resistance in hypertensive subjects can be reduced by centrally inhibiting sympathetic overactivity with dexamethasone. Coronary vascular resistance was quantitated in 11 men with untreated mild essential hypertension (RR 149 +/- 13/98 +/- 10 mm Hg) and 23 healthy, normotensive, otherwise matched men using positron emission tomography and [(15)O]H(2)O. The measurements were performed at baseline and during adenosine stimulation. Each subject was studied twice, with and without previous dexamethasone treatment for two days (0.5 mg x 4 per day). Before dexamethasone treatment, cardiac index and plasma norepinephrine concentration (1.9 +/- 0.6 vs. 1.3 +/- 0.5 nmol/l, p < 0.01) were significantly higher in hypertensive than in normotensive subjects. Additionally, both baseline and hyperemic coronary vascular resistances were higher in hypertensive than normotensive subjects (147 +/- 31 vs. 113 +/- 24 and 36 +/- 9 vs. 25 +/- 10 mm Hg.min.g.ml(-1); p < 0.05). Dexamethasone treatment significantly decreased plasma norepinephrine concentrations in hypertensive subjects, leading to comparable plasma norepinephrine concentrations in hypertensive and normotensive subjects (1.4 +/- 0.5 vs. 1.2 +/- 0.4 nmol/l; NS). However, coronary vascular resistances remained increased in hypertensive subjects. In conclusion, hypertensive subjects are characterized by sympathetic overactivity, which can be normalized by dexamethasone. However, coronary vascular resistances remained increased in hypertensive subjects after dexamethasone treatment, suggesting that other mechanisms than sympathetic overactivity-induced vasoconstriction explain the increased coronary vascular resistance in hypertension.
Authors:
Jan Sundell; Hanna Laine; Matti Luotolahti; Pirjo Nuutila; Juhani Knuuti
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of vascular research     Volume:  39     ISSN:  1018-1172     ISO Abbreviation:  J. Vasc. Res.     Publication Date:    2002 Sep-Oct
Date Detail:
Created Date:  2002-09-25     Completed Date:  2002-11-04     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  9206092     Medline TA:  J Vasc Res     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  456-62     Citation Subset:  IM    
Copyright Information:
Copyright 2002 S. Karger AG, Basel
Affiliation:
Turku PET Centre, Turku University, Turku, Finland. jan.sundell@utu.fi
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MeSH Terms
Descriptor/Qualifier:
Adult
Blood Glucose / analysis
Coronary Circulation / drug effects
Coronary Vessels / drug effects*
Dexamethasone / therapeutic use*
Female
Glucocorticoids / therapeutic use*
Hemodynamics
Humans
Hydrocortisone / blood
Hypertension / drug therapy*,  physiopathology
Male
Norepinephrine / blood
Tomography, Emission-Computed
Vascular Resistance / drug effects*
Chemical
Reg. No./Substance:
0/Blood Glucose; 0/Glucocorticoids; 50-02-2/Dexamethasone; 50-23-7/Hydrocortisone; 51-41-2/Norepinephrine

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