PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
14644762-7	2004	The effect of lisinopril was prevented by pretreatment with a bradykinin antagonist (HOE-130) and dichloroisocoumarine, an inhibitor of kinine-forming enzymes.	Lisinopril	14-24	kininogen 1	Homo sapiens	62-72	
11410114-12	2001	The mechanism could be either that lisinopril limits the angiotensin II-induced production of superoxide radicals which would normally inactivate NO, or that lisinopril may increase bradykinin-mediated NO release.	Lisinopril	158-168	kininogen 1	Homo sapiens	182-192	
8386065-7	1993	Bradykinin concentrations in the organ bath measured by a specific bradykinin radioimmunoassay remained stable during the addition of lisinopril.	Lisinopril	134-144	kininogen 1	Homo sapiens	0-10	
10703672-7	2000	In the third series, lisinopril reduced BP from 121 +/- 5 to 68 +/- 2 mmHg and proteinuria from 355 +/- 90 to 101 +/- 10 mg/24 h. Subsequent intraperitoneal infusion of bradykinin antagonist (HOE 140; 1 mg/kg per 24 h) for 2 wk did not affect BP (72 +/- 2 mmHg) or proteinuria (92 +/- 15 mg/24 h).	Lisinopril	21-31	kininogen 1	Homo sapiens	169-179	
9797190-8	1998	However, when the responses to infusions of acetylcholine and bradykinin were normalized with respect to that to infusion of sodium nitroprusside, only the vasodilatation in response to infusion of bradykinin was shown to have been increased by lisinopril treatment.	Lisinopril	245-255	kininogen 1	Homo sapiens	198-208	
9797190-9	1998	CONCLUSIONS: Administration of lisinopril to patients with essential hypertension can selectively increase vasodilatation in response to infusion of bradykinin.	Lisinopril	31-41	kininogen 1	Homo sapiens	149-159	
11247797-7	2001	Simultaneous with kallikrein formation, bradykinin (5.0 or 10.3 pmol/10(6) HUVEC in the absence or presence of lisinopril, respectively) is liberated from cell-bound HK.	Lisinopril	111-121	kininogen 1	Homo sapiens	40-50	
10535387-2	1999	In the present study, we measured plasma levels of nitric oxide (NO) and the related vasoactive factors bradykinin, 6-keto prostaglandin F1alpha (6-keto PGF1alpha) a stable metabolite of prostacyclin, and cyclic guanosine-3",5"-monophosphate (cGMP) before and after a 4-week treatment with the ACE inhibitor lisinopril in 17 patients with essential hypertension.	Lisinopril	308-318	kininogen 1	Homo sapiens	104-114	
9797190-6	1998	Acute and prolonged lisinopril treatments significantly (P < 0.05 or less) improved vasodilatation in response to infusion of bradykinin (from 3.7 +/- 0.4 to 24.5 +/- 4.9 and from 3.7 +/- 0.3 to 22.1 +/- 4.9 ml/100 ml per min, respectively), but not in response to infusions of acetylcholine and of sodium nitroprusside.	Lisinopril	20-30	kininogen 1	Homo sapiens	129-139	
9797190-7	1998	Chronic lisinopril treatment increased (P < 0.05) the response to infusions of not only bradykinin (from 3.5 +/- 0.5 to 27.6 +/- 5.3 ml/100 ml per min), but also of acetylcholine (from 3.5 +/- 0.5 to 27.8 +/- 8.0 ml/100 ml per min) and sodium nitroprusside (from 3.4 +/- 0.6 to 25.9 +/- 8.5 ml/100 ml per min).	Lisinopril	8-18	kininogen 1	Homo sapiens	91-101	
8388656-3	1993	Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisinopril, ramiprilat, and captopril.	Lisinopril	138-148	kininogen 1	Homo sapiens	12-22	
8395230-6	1993	The angiotensin-converting enzyme inhibitor, lisinopril (10(-8) mol/l), increased the half-life of bradykinin to 244 +/- 20 minutes; the combination of both inhibitors increased the half-life of bradykinin to 381 +/- 51 minutes.	Lisinopril	45-55	kininogen 1	Homo sapiens	99-109	
8395230-6	1993	The angiotensin-converting enzyme inhibitor, lisinopril (10(-8) mol/l), increased the half-life of bradykinin to 244 +/- 20 minutes; the combination of both inhibitors increased the half-life of bradykinin to 381 +/- 51 minutes.	Lisinopril	45-55	kininogen 1	Homo sapiens	195-205	
8386065-11	1993	Endothelium dependent relaxation to lisinopril and captopril was also observed in human coronary arteries treated with bradykinin (> or = 10(-7) M), but not in those treated with substance P (10(-8) M).	Lisinopril	36-46	kininogen 1	Homo sapiens	119-129	
1282632-6	1992	Mechanical removal of the endothelium or incubation with nitro-L-arginine or the bradykinin2-receptor antagonist Hoe 140 prevented the relaxations to bradykinin and lisinopril.	Lisinopril	165-175	kininogen 1	Homo sapiens	81-91	
1282632-8	1992	Endothelium-dependent relaxations to lisinopril were also observed in human coronary arteries treated with bradykinin (> or = 10(-7) M).	Lisinopril	37-47	kininogen 1	Homo sapiens	107-117	
22200082-5	2012	ACE activity was assayed by monitoring cleavage of the fluorogenic substrate Mca-RPPGFSAFK(Dnp)-OH, a derivative of bradykinin, following preincubation with metal chelate-lisinopril compounds.	Lisinopril	171-181	kininogen 1	Homo sapiens	116-126	
18084312-5	2008	In the presence of lisinopril (ACE inhibitor), but not candoxatril (NEP inhibitor) or apstatin (APP inhibitor), bradykinin also elicited hypotension.	Lisinopril	19-29	kininogen 1	Homo sapiens	112-122