Planta Med 2000; 66(7): 601-606
DOI: 10.1055/s-2000-8625
Original Paper
Georg Thieme Verlag Stuttgart · New York

Kavain Inhibits Murine Airway Smooth Muscle Contraction

Hugh B. Martin*, William D. Stofer, Mark R. Eichinger
  • Department of Anesthesiology, University of New Mexico Health Sciences Center, Albuquerque, N.M., U.S.A.
Further Information

Publication History

Publication Date:
31 December 2000 (online)

Abstract

This study examined the effect of kavain, the principle biologically active component of kava, on murine airway smooth muscle. In isolated isometrically contracted tracheal ring preparations, kavain was noted to diminish the maximal contractile response to both muscarinic receptor activation and voltage-operated calcium channel activation. The IC50 for kavain in rings precontracted with carbachol was found to be 177 μM ± 53.1, and, in rings precontracted with KCl, it was found to be 59.6 μM ± 10.1. In addition, pretreatment with kavain attenuated airway smooth muscle contraction evoked with either carbachol or KCl. The EC50 for KCl was not affected by kavain pretreatment. However, the EC50 for carbachol was significantly affected by a high kavain pretreatment dose. Nitric oxide mediated relaxation was not observed to play a role in kavain's smooth muscle relaxing properties. Similarly, prostaglandin pathways are not likely involved in these effects since pretreatment of tracheal rings with indomethacin before carbachol contraction did not reduce the relaxant effect of kavain. The mechanism of kavain-induced relaxation and inhibition of contraction is likely due to a mechanism common to both contractile agonists that were employed in our study.

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M.D. Hugh B. Martin

Department of Anesthesiology School of Medicine University of New Mexico Health Sciences Center

Surge Building

Albuquerque, N.M. 87131

U.S.A.

Email: hmartin@salud.unm.edu

Phone: +1 505-272-1300

Fax: +1 505-272-4757

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