PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
8242234-3	1993	Although a number of investigators have evaluated angiotensin-converting enzyme (ACE) activity in the lungs of rats treated with MCT, the exact nature of changes in activity of this enzyme and the role they may play in MCT pneumotoxicity remain controversial.	Monocrotaline	129-132	angiotensin I converting enzyme	Rattus norvegicus	81-84	
7954654-1	1994	OBJECTIVE: The aim was to examine the effects of an angiotensin converting enzyme (ACE) inhibitor and a calcium antagonist on intracellular calcium transients in isolated cardiac myocytes from a monocrotaline induced right ventricular hypertrophy model.	Monocrotaline	195-208	angiotensin I converting enzyme	Rattus norvegicus	83-86	
9296348-1	1997	Alterations in lung angiotensin converting enzyme (ACE) activity in monocrotaline (MCT)-induced pulmonary hypertension in rats have suggested a pathophysiologic role for angiotensin II (AII) in pulmonary vascular remodeling.	Monocrotaline	68-81	angiotensin I converting enzyme	Rattus norvegicus	20-49	
9296348-1	1997	Alterations in lung angiotensin converting enzyme (ACE) activity in monocrotaline (MCT)-induced pulmonary hypertension in rats have suggested a pathophysiologic role for angiotensin II (AII) in pulmonary vascular remodeling.	Monocrotaline	68-81	angiotensin I converting enzyme	Rattus norvegicus	51-54	
9296348-1	1997	Alterations in lung angiotensin converting enzyme (ACE) activity in monocrotaline (MCT)-induced pulmonary hypertension in rats have suggested a pathophysiologic role for angiotensin II (AII) in pulmonary vascular remodeling.	Monocrotaline	83-86	angiotensin I converting enzyme	Rattus norvegicus	20-49	
9296348-1	1997	Alterations in lung angiotensin converting enzyme (ACE) activity in monocrotaline (MCT)-induced pulmonary hypertension in rats have suggested a pathophysiologic role for angiotensin II (AII) in pulmonary vascular remodeling.	Monocrotaline	83-86	angiotensin I converting enzyme	Rattus norvegicus	51-54	
8242234-5	1993	We examined the direct effects of monocrotaline pyrrole (MCTP), a toxic metabolite of MCT, on cultured endothelial cell ACE activity.	Monocrotaline	57-60	angiotensin I converting enzyme	Rattus norvegicus	120-123	
3035737-6	1986	Lung angiotensin converting enzyme activity was decreased after three days" ingestion of monocrotaline and did not alter further with longer periods of exposure.	Monocrotaline	89-102	angiotensin I converting enzyme	Rattus norvegicus	5-34	
2994075-11	1985	Neither modifying agent influenced the monocrotaline-induced decrease in lung ACE activity.	Monocrotaline	39-52	angiotensin I converting enzyme	Rattus norvegicus	78-81	
2994075-15	1985	Perhaps more importantly, the hydroxyproline data demonstrate that the ACE inhibitor Captropril exhibits antifibrotic activity in monocrotaline-treated rat lung.	Monocrotaline	130-143	angiotensin I converting enzyme	Rattus norvegicus	71-74	
6324229-2	1984	Lung ACE activity increased after 1 week of monocrotaline, then decreased steadily from 1 to 6 weeks, before plateauing at approximately 55% of normal.	Monocrotaline	44-57	angiotensin I converting enzyme	Rattus norvegicus	5-8	
27344167-10	2016	In conclusion, monocrotaline-induced PH exhibited similar alterations of ACE expression in the left and right ventricles, and in the kidney, in contrast to the lungs.	Monocrotaline	15-28	angiotensin I converting enzyme	Rattus norvegicus	73-76	
2547380-9	1989	These monocrotaline-induced structural changes were accompanied by decreased lung ACE and PLA activities, and increased PGI2 and TXA2 production, and by an increase in lung hydroxyproline content.	Monocrotaline	6-19	angiotensin I converting enzyme	Rattus norvegicus	82-85	
3129998-1	1988	Thiol angiotensin converting enzyme (ACE) inhibitors (Captopril, CL242817) and collagen antagonists (D-penicillamine) partially prevent pulmonary hypertension in monocrotaline-treated rats.	Monocrotaline	162-175	angiotensin I converting enzyme	Rattus norvegicus	6-35	
3129998-1	1988	Thiol angiotensin converting enzyme (ACE) inhibitors (Captopril, CL242817) and collagen antagonists (D-penicillamine) partially prevent pulmonary hypertension in monocrotaline-treated rats.	Monocrotaline	162-175	angiotensin I converting enzyme	Rattus norvegicus	37-40	
3129998-6	1988	Monocrotaline-induced histopathologic changes in the lung were accompanied by pulmonary endothelial dysfunction, including suppressed ACE and plasminogen activator activity and increased prostacyclin and thromboxane production.	Monocrotaline	0-13	angiotensin I converting enzyme	Rattus norvegicus	134-137