Suppression of alcohol-induced hypertension by dexamethasone

Détails

Ressource 1Télécharger: 5_7760888.pdf (629.64 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_32548B9D5394
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Suppression of alcohol-induced hypertension by dexamethasone
Périodique
New England Journal of Medicine
Auteur(s)
Randin  D., Vollenweider  P., Tappy  L., Jequier  E., Nicod  P., Scherrer  U.
ISSN
0028-4793 (Print)
Statut éditorial
Publié
Date de publication
06/1995
Volume
332
Numéro
26
Pages
1733-7
Notes
Clinical Trial
Controlled Clinical Trial
Journal Article
Randomized Controlled Trial
Research Support, Non-U.S. Gov't --- Old month value: Jun 29
Résumé
BACKGROUND. Alcohol consumption is associated with an increased incidence of hypertension and stroke, but the triggering mechanisms are unclear. In animals, alcohol causes activation of the sympathetic nervous system and also stimulates the release of corticotropin-releasing hormone (CRH), which has sympatho-excitatory effects when administered centrally. METHODS. To determine whether alcohol evokes sympathetic activation and whether such activation is attenuated by the inhibition of CRH release, we measured blood pressure, heart rate, and sympathetic-nerve action potentials (using intraneural microelectrodes) in nine normal subjects before and during an intravenous infusion of alcohol (0.5 g per kilogram of body weight over a period of 45 minutes) and for 75 minutes after the infusion. Each subject received two infusions, one after the administration of dexamethasone (2 mg per day) and one after the administration of a placebo for 48 hours. RESULTS. The infusion of alcohol alone evoked a marked (P < 0.001) and progressive increase in the mean (+/- SD) rate of sympathetic discharge, from 16 +/- 3 bursts per minute at base line to 30 +/- 8 bursts per minute at the end of the two-hour period. This sympathetic activation was accompanied during the second hour by an increase in mean arterial pressure of 10 +/- 5 mm Hg (P < 0.001). After the administration of dexamethasone, the alcohol infusion had no detectable sympathetic effect. The dexamethasone-induced suppression of sympathetic activation was associated with a decrease in mean arterial pressure of 7 +/- 6 mm Hg (P < 0.001) during the alcohol infusion and with suppression of the pressor effect during the second hour. CONCLUSIONS. Alcohol induces pressor effects by sympathetic activation that appear to be centrally mediated. It is possible that these alcohol-induced hemodynamic and sympathetic actions could participate in triggering cardiovascular events.
Mots-clé
Action Potentials Adult Blood Pressure/drug effects Corticotropin-Releasing Hormone/secretion Dexamethasone/*pharmacology Double-Blind Method Ethanol/*pharmacology Female Hemodynamic Processes/drug effects Humans Hypertension/chemically induced/*physiopathology Infusions, Intravenous Male Phentolamine/pharmacology Sympathetic Nervous System/*drug effects
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 14:36
Dernière modification de la notice
20/08/2019 14:17
Données d'usage