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EFFECT OF PROPOFOL ON VASOCONSTRICTION AND CALCIUM MOBILIZATION INDUCED BY ANGIOTENSIN II DIFFERS IN AORTAS FROM NORMOTENSIVE AND HYPERTENSIVE RATS
Author(s) -
Samain Emmanuel,
PiliFloury Sébastien,
Bouillier Hélène,
Clichet Adeline,
Safar Michel,
Dagher Georges,
Marty Jean,
Renaud JeanFrançois
Publication year - 2004
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2004.03968.x
Subject(s) - propofol , angiotensin ii , isometric exercise , medicine , vasoconstriction , endocrinology , blood pressure , renin–angiotensin system , chemistry , anesthesia
SUMMARY 1. Angiotensin (Ang) II is a potent vasopressor agent, involved in the short‐term control of arterial blood pressure during anaesthesia. The aim of the present study was to test the hypothesis that propofol, a widely used intravenous anaesthetic agent, could alter the arterial response to AngII and to evaluate its effect in genetic hypertension. 2. We studied the effect of increasing concentrations of propofol (5.6 × 10 −7 to 5.6 × 10 −4  mol/L) on aortic ring maximal isometric tension elicited by AngII and on AngII‐induced Ca 2+ mobilization in aortic smooth muscle cells from Wistar‐Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). 3. Maximal tension developed by aortic rings from WKY rats was greater than that developed by rings from SHR. In both WKY rats and SHR, propofol at concentrations from 5.6 × 10 −6  mol/L decreased maximal tension induced by AngII in a concentration‐dependent manner. The magnitude of inhibition was higher in SHR than in WKY rats, whereas pD 2 values were not different. In addition, Ca 2+ mobilization induced by AngII was inhibited by propofol in a concentration‐dependent manner, with the same magnitude and pD 2 values. 4. These results suggest that the arterial response to AngII may be altered during propofol anaesthesia, particularly in hypertension.

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