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CARDIOVASCULAR ANESTHESIA

The Effect of Propofol on Angiotensin II-Induced Ca²⁺ Mobilization in Aortic Smooth Muscle Cells from Normotensive and Hypertensive Rats

Emmanuel Samain, MD, PhD^*, Hélène Bouillier, Jean Marty, MD^*, Michel Safar, MD, PhD, and Georges Dagher, PhD

*Department of Anesthesiology, Beaujon Hospital, University Xavier Bichat, Clichy; and INSERM U337, Paris, France

Address correspondence and reprint requests to Emmanuel Samain, MD, PhD, Department of Anesthesiology, Beaujon Hospital, University Xavier Bichat, 100 Blvd. General Leclerc, 92110 Clichy, France.

We studied the effect of propofol (5.6–560 µmol/L; 1–100 µg/mL) on the mechanisms involved in Ca²⁺ mobilization elicited by angiotensin II (AngII) in Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. We studied the variations in intracellular Ca²⁺ ([Ca²⁺]_i) concentrations in cultured aortic vascular smooth muscle cells (VSMCs) isolated from 6-wk-old WKY and SHR rats loaded with the Ca²⁺-sensitive fluorescent dye, Fura-2, using fluorescent imaging microscopy. In the absence of external Ca²⁺, AngII (1 µmol/L) induced a transient [Ca²⁺]_i mobilization from internal stores that was larger in SHR than in WKY rats. Ca²⁺ influx was assessed after external Ca²⁺ (1 mmol/L) reintroduction. Propofol (1–100 µg/mL) added 5 min before the experiments did not alter AngII-induced Ca²⁺ release from internal stores in either strain. By contrast, Ca²⁺ influx elicited by AngII was significantly decreased by propofol. This effect occurred at a smaller concentration of propofol in the SHR than in the WKY rats. When Ca²⁺ stores were depleted by exposure of cells to thapsigargin, an inhibitor of the sarcoendoplasmic reticulum Ca²⁺-ATPase, reintroduction of Ca²⁺ to the medium induced a capacitative Ca²⁺ influx of similar magnitude than that elicited by AngII. This influx was also significantly decreased by propofol at 100 µg/mL (

WKY: 27 ± 3% of control values, n = 107;

SHR: 16 ± 3%, n = 47; P < 0.001). In conclusion, propofol decreased AngII-induced Ca²⁺ influx through voltage-independent channels, without altering Ca²⁺ release from internal stores in aortic VSMCs. The hypertensive rats were found to be more sensitive to the effect of propofol than the normotensive rats. This suggests that the response of VSMCs to AngII may be altered by propofol.

Implications: In rat aortic vascular smooth muscle cells, propofol reduced angiotensin II-elicited Ca²⁺ entry through capacitative Ca²⁺ channels without altering Ca²⁺ release from intracellular stores. Spontaneously hypertensive rats were more sensitive to these effects of propofol than normotensive rats. The response of vascular smooth muscle cells to angiotensin II may be altered by propofol.

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