Titre
Angiotensin I conversion and vascular reactivity in pathophysiological states in dogs
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Auteur(s)
Leuenberger, P. J.
Auteure/Auteur
Stalcup, S. A.
Auteure/Auteur
Greenbaum, L. M.
Auteure/Auteur
Mellins, R. B.
Auteure/Auteur
Turino, G. M.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
0161-7567
Statut éditorial
Publié
Date de publication
1980-02
Volume
48
Numéro
2
Première page
308
Dernière page/numéro d’article
12
Notes
Journal Article
Research Support, U.S. Gov't, P.H.S. --- Old month value: Feb
Research Support, U.S. Gov't, P.H.S. --- Old month value: Feb
Résumé
To determine if angiotension converting enzyme activity is altered by acute pathophysiological insults, we assessed angiotensin I conversion using a blood pressure response technique in anesthetized dogs studied during acute 100% O2 breathing and acute acid-base derangements. Also, we determined systemic vascular reactivity to angiotensin II by measuring the magnitude and duration of the arterial blood pressure response to intra-arterial injections of angiotensin II under these same conditions. Angiotensin I conversion found in normoxia [91 +/- 7 (SD)%] was unchanged by acute acidosis, alkalosis, and hyperoxia. During acute hyperoxia the mean half time of the hypertensive response increased from 68 +/- 25 (SD) s at a PaO2 of 112 +/- 18 (SD) Torr to 100 +/- 34 (SD) s at a PaO2 of 491 +/- 47 (SD) Torr (P less than 0.01). No other pathophysiological condition studied had any effect on reactivity of systemic vasculature to angiotensin II. We conclude that, except during acute hypoxia as previously shown, converting enzyme activity is resistant to other pathophysiological insults and that vascular responsiveness to angiotensin II is enhanced by hyperoxia.
Sujets
PID Serval
serval:BIB_CBF0E31F82C8
PMID
Date de création
2008-01-25T08:50:24.504Z
Date de création dans IRIS
2025-05-21T02:02:21Z