PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
1333254-1	1992	In the present studies, ex vivo-, in vitro-, and in vivo-effects of three structurally different angiotensin I-converting enzyme (ACE) inhibitors on the kallikrein-kinin and eicosanoid systems are described.	Eicosanoids	174-184	angiotensin I converting enzyme	Homo sapiens	97-128	
8292107-5	1993	Laboratory investigations of hepatic effects of eicosanoids on hepatic function are reviewed and a novel mechanism by which ACE inhibitors may cause hepatic injury is postulated.	Eicosanoids	48-59	angiotensin I converting enzyme	Homo sapiens	124-127	
8292107-8	1993	Potential mechanisms of injury include idiopathic hypersensitivity and modulation of eicosanoid metabolism by inhibition of kininase II and subsequent increased hepatic bradykinin activity.	Eicosanoids	85-95	angiotensin I converting enzyme	Homo sapiens	124-135	
8292107-9	1993	Mediation via altered eicosanoid metabolism provides a plausible explanation for cross-reactivity among ACE inhibitors.	Eicosanoids	22-32	angiotensin I converting enzyme	Homo sapiens	104-107	
2483428-6	1989	These data indicate that human arterial SMCs may express several phenotypes of the renin-angiotensin system under culture conditions and that ACE inhibitors may exert a non-renin-angiotensin-mediated pharmacological effect on eicosanoid synthesis.	Eicosanoids	226-236	angiotensin I converting enzyme	Homo sapiens	142-145