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Activation of the K+ channel BKCa is involved in the relaxing effect of propofol on coronary arteries

Published online by Cambridge University Press:  23 December 2004

A. P. Klockgether-Radke
Affiliation:
Georg-August University of Göttingen, Centre of Anaesthesiology, Emergency and Intensive Care Medicine, Göttingen, Germany
H. Schulze
Affiliation:
Georg-August University of Göttingen, Centre of Anaesthesiology, Emergency and Intensive Care Medicine, Göttingen, Germany
P. Neumann
Affiliation:
Georg-August University of Göttingen, Centre of Anaesthesiology, Emergency and Intensive Care Medicine, Göttingen, Germany
G. Hellige
Affiliation:
Georg-August University of Göttingen, Centre of Anaesthesiology, Emergency and Intensive Care Medicine, Göttingen, Germany
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Abstract

Summary

Background and objective: Propofol may cause undesirable hypotension due to vasodilation. The underlying mechanisms are not completely understood. We investigated the mechanisms by which propofol relaxes vascular segments.

Methods: We studied the effect of propofol on isolated porcine coronary artery rings precontracted with potassium chloride or prostaglandin F.

Results: Propofol, in a concentration-dependent manner, relaxed all segments at concentrations of 5 μg mL−1 and above. This relaxation was unaltered in the presence of Nω-nitro-L-arginine, indomethacin, diltiazem and glibenclamide. Tetraethylammonium chloride, an inhibitor of the BKCa K+ channel (a high conductance Ca2+-sensitive K+ channel), dose-dependently attenuated the vasodilating effect of propofol (P < 0.001).

Conclusions: Our results suggests that the activation of the BKCa channel may contribute to the vasodilating effect of propofol, hereby causing hyperpolarization of the smooth muscle membrane and reduction of smooth muscle tone.

Type
Original Article
Copyright
2004 European Society of Anaesthesiology

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