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Title of Journal: J Anesth

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Abbravation: Journal of Anesthesia

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Springer Japan

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DOI

10.1007/s12027-010-0182-8

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1438-8359

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Effects of amitriptyline a tricyclic antidepressa

Authors: Shoji Matsunaga Osamu Shibata Kenji Nishioka Atsushi Tsuda Tetsuji Makita Koji Sumikawa
Publish Date: 2009/08/14
Volume: 23, Issue: 3, Pages: 385-391
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Abstract

In isolated rat trachea isometric force was recorded to examine the effects of amitriptyline on the contractile response to acetylcholine ACh electrical field stimulation EFS calyculin A a myosin light chain phosphatase inhibitor and sphingosylphosphorylcholine SPC a Rhokinase activator In addition inositol monophosphate IP1 accumulation was measured to examine its effects on inositol 1 4 5trisphosphate IP3 production during stimulation with AChAmitriptyline inhibited the contractile responses to ACh EFS calyculin A and SPC with the concentrations of amitriptyline mean ± SD required to exert 50 inhibition IC50 being 43 ± 13 μM 32 ± 16 μM 2564 ± 1064 μM and 982 ± 218 μM respectively In addition amitriptyline 10 μM eliminated the ACh 10 μMinduced IP1 accumulationThe results suggest that amitriptyline does not influence tracheal smooth muscle reactivity at clinical concentrations 1 μM but attenuates the reactivity at supraclinical concentrations ≥1 μM The attenuated response to ACh brought about by amitriptyline is presumably due at least in part to the inhibition of phosphatidylinositol PI metabolism The ability of amitriptyline to inhibit the calyculin Ainduced contraction suggests that amitriptyline also inhibits the Ca2+calmodulinmyosin light chain pathway independently of the inhibition of PI metabolism Finally the difference between the IC50 values for SPCinduced contraction and those for calyculin Ainduced contraction suggests that amitriptyline may also inhibit the Rhokinase pathway

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