TREATMENT IN THE NARCOLEPTIC SYNDROME - SELF-ASSESSMENT OF THE ACTION OF DEXAMPHETAMINE AND CLOMIPRAMINE

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Title:	TREATMENT IN THE NARCOLEPTIC SYNDROME - SELF-ASSESSMENT OF THE ACTION OF DEXAMPHETAMINE AND CLOMIPRAMINE
Authors:	CHEN, SY;CLIFT, SJ;DAHLITZ, MJ;DUNN, G;PARKES, JD
Contributors:	附設醫院精神醫學部;CHINA MED COLL HOSP,DEPT PSYCHIAT,TAICHUNG,TAIWAN;UNIV LONDON KINGS COLL,SCH MED & DENT,DEPT NEUROL,LONDON WC2R 2LS,ENGLAND;INST PSYCHIAT,DEPT BIOSTAT & COMP,LONDON,ENGLAND
Date:	1995
Issue Date:	2010-09-24 14:51:54 (UTC+8)
Publisher:	BLACKWELL SCIENCE LTD
Abstract:	Butein, isolated from Dalbergia odorifera T. Chen, caused endothelium-dependent relaxation of rat aorta precontracted with phenylephrine. This effect was abolished in endothelium-denuded aorta and in endothelium-intact aorta in the presence of N-G-monomethyl-L-arginine, oxyhemoglobin and methylene blue, whereas the effect was unaltered by indomethacin or charybdotoxin, These results indicate that the vasorelaxant effect of butein depended on the endothelium and was mediated by endothelium-derived relaxing factor (EDRF). Incubation of endothelium-intact aorta with butein increased not only cAMP but also cGMP content. Four phosphodiesterase forms were isolated by diethylaminoethyl (DEAE)-Sephacel chromatography from rat aorta. cAMP-specific phosphodiesterase (type IV) activity was potently inhibited by butein with an IC50 of 10.4 +/- 0.4 mu M. In contrast, phosphodiesterase I, III and V activities were inhibited by butein above 100 mu M. Adenylate cyclase and guanylate cyclase activities were unchanged by butein. These results suggest that the increase of cAMP formation elicited by butein is due to the inhibition of cAMP-specific phosphodiesterase. The specific phosphodiesterase IV inhibitor (rolipram) and V inhibitor (zaprinast) both produced endothelium-dependent relaxations, whereas the phosphodiesterase III inhibitor (trequinsin) produced relaxation of rat aorta independent of the endothelium. In the presence of a functional endothelium, relaxations produced by butein were significantly potentiated by isoprenaline, forskolin, trequinsin and sodium nitroprusside. It is concluded that butein, a novel cAMP-specific phosphodiesterase inhibitor, produced relaxation of rat aorta, an effect dependent on an intact endothelium. The relaxant effect of butein was markedly enhanced by cGMP-elevating agents. These results indicated that cGMP enhances cAMP-mediated relaxation possibly through the inhibition of the cGMP-inhibited cAMP phosphodiesterase.
Relation:	JOURNAL OF SLEEP RESEARCH 4(2):113-118
Appears in Collections:	[China Medical University Hospital] Jurnal articles

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