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British Journal of Anaesthesia, 2000, Vol. 85, No. 6 874-880
© 2000 The Board of Management and Trustees of the British Journal of Anaesthesia

Inhibitory effects of intravenous anaesthetic agents on K+-evoked norepinephrine and dopamine release from rat striatal slices: possible involvement of P/Q-type voltage-sensitive Ca2+ channels

K. Hirota1, M. Kudo1, T. Kudo1, A. Matsuki1 and D. G. Lambert2

1Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki 036-8562, Japan. 2University Department of Anaesthesia and Pain Management, Leicester Royal Infirmary, Leicester LE1 5WW, UK*Corresponding author

The role of the voltage-sensitive Ca2+ channel (VSCC) as a target for anaesthetic action remains controversial. In this study we characterized the VSCC subtypes involved in K+-evoked norepinephrine and dopamine release from rat striatal slices and used this model system to examine the effects of a range of i.v. anaesthetics on release. Nifedipine (L-channel-selective), {omega}-conotoxin GVIA (N-channel-selective), {omega}-agatoxin IVA (P-channel-selective), {omega}-conotoxin MVIIC (P/Q-channel-selective) and Cd2+ (non-selective), along with alphaxalone, propofol and ketamine, were used in various combinations. {omega}-Agatoxin IVA, {omega}-conotoxin MVIIC and Cd2+ fully (100%) inhibited norepinephrine and dopamine release. Clinically achievable concentrations of alphaxalone inhibited norepinephrine and dopamine release, with concentrations producing 25 and 50% inhibition (IC25 and IC50) of the maximum of 2.1 and 7.8 µM respectively for norepinephrine and 2.9 and 7.2 µM for dopamine. The effects of propofol were observed at the top of the clinical range and those of ketamine exceeded this range. In addition, IC50 values for alphaxalone in the presence and absence of nifedipine and {omega}-conotoxin GVIA did not differ from the control. Our data suggest that clinically achievable concentrations of alphaxalone and propofol inhibit norepinephrine and dopamine release, which is mediated predominantly through P/Q-type VSCCs, suggesting a role for these channels in anaesthetic action.

Br J Anaesth 2000; 85: 874–80


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