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British Journal of Anaesthesia, Vol 81, Issue 4 578-583, Copyright © 1998 by The Board of Management and Trustees of the British Journal of Anaesthesia

LABORATORY INVESTIGATIONS

Effects of isoflurane on receptor-operated Ca2+ channels in rat aortic smooth muscle

S. Hirata, T. Enoki, R. Kitamura, V. H. Vinh, K. Nakamura and K. Mori
Department of Anaesthesia, Kyoto University Hospital, Kyoto 606-8507, Japan; Department of Anaesthesia, Kyoto City Hospital, Kyoto 604, Japan

We have investigated the effects of isoflurane on receptor-operated Ca2+ channels (ROC) in vascular smooth muscle. In isolated rat thoracic aortic rings denuded of endothelium, the effects of isoflurane on phenylephrine-induced contraction and Ca2+ influx were evaluated in the presence of supramaximal doses of nifedipine or verapamil. Under isometric tension recording, the aortic rings were precontracted by phenylephrine 300 nmol litre-1 and exposed to 1.2%, 2.3% or 3.5% isoflurane. Phenylephrine-induced precontraction was enhanced with 2.3% isoflurane by mean 8.1 (SD 9.3)% (P < 0.05 vs 0% isoflurane). The constrictor effect of 2.3% isoflurane was not inhibited by depletion of intracellular Ca2+ stores with ryanodine 20 microgramsmol litre-1, but was abolished in a Ca(2+)-free solution or by SK&F 96,365 30 microgramsmol litre-1, an ROC blocker. Isoflurane-induced contraction was accompanied by increased intracellular free Ca2+ concentration, monitored using fura PE3. Unidirectional 45Ca2+ influx measurement in phenylephrine- stimulated aortic strips revealed that the mean amount of Ca2+ influx was significantly (P < 0.05) enhanced by 1.2% and 2.3% isoflurane, which were 117.1% and 119.7% of control values, respectively. Our results strongly suggest that isoflurane enhanced Ca2+ influx through ROC that had been submaximally activated by phenylephrine.
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