PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
8930174-8	1996	Both ACE inhibitors dramatically, equally potentiated the vasodepressor response to bradykinin; the bradykinin dose required to decrease mean arterial pressure 15 mm Hg or increase pulse 20 bpm was 50-fold lower in ACEI-treated than in placebo-treated subjects (10 +/- 0 and 12.1 +/- 2.1 ng/kg/min in captopril and quinapril groups vs. 567 +/- 109 ng/kg/min in the placebo group; P < .005).	Quinapril	315-324	kininogen 1	Homo sapiens	100-110	
10604961-8	2000	Pretreatment with 10 mg of quinapril significantly shifted the dose-response curve for bradykinin to the left (effect of quinapril; F = 77.96, P <.001) and there was significant interaction between quinapril and bradykinin (F = 7.82, P =.041).	Quinapril	27-36	kininogen 1	Homo sapiens	87-97	
10604961-8	2000	Pretreatment with 10 mg of quinapril significantly shifted the dose-response curve for bradykinin to the left (effect of quinapril; F = 77.96, P <.001) and there was significant interaction between quinapril and bradykinin (F = 7.82, P =.041).	Quinapril	27-36	kininogen 1	Homo sapiens	215-225	
10604961-8	2000	Pretreatment with 10 mg of quinapril significantly shifted the dose-response curve for bradykinin to the left (effect of quinapril; F = 77.96, P <.001) and there was significant interaction between quinapril and bradykinin (F = 7.82, P =.041).	Quinapril	121-130	kininogen 1	Homo sapiens	87-97	
10604961-8	2000	Pretreatment with 10 mg of quinapril significantly shifted the dose-response curve for bradykinin to the left (effect of quinapril; F = 77.96, P <.001) and there was significant interaction between quinapril and bradykinin (F = 7.82, P =.041).	Quinapril	121-130	kininogen 1	Homo sapiens	87-97	
10604961-9	2000	The effect of quinapril was significantly potentiated by coinjection of 10 microg of apstatin (effect of apstatin; F = 21.60, P =.006), such that there was significant interactive effect of quinapril and apstatin (F = 20.83, P =.006) on the wheal response to bradykinin.	Quinapril	14-23	kininogen 1	Homo sapiens	259-269	
9066005-4	1997	Bradykinin was infused in seventeen hypertensive patients randomized to treatment with the ACEIs captopril and quinapril or with placebo.	Quinapril	111-120	kininogen 1	Homo sapiens	0-10	
11986905-10	2002	This proposal is supported by different clinical trials that have shown that the ACE inhibitors with higher affinity by the tissular ACE, such as quinapril, are the most effective in reversing ED principally by accumulating bradykinin.	Quinapril	146-155	kininogen 1	Homo sapiens	224-234	
20631409-12	2010	The thrombolytic actions of lipophilic ACE-Is (e.g., quinapril and perindopril) were prevented by pretreatment with either bradykinin B(2) receptor antagonists (e.g., icatibant) or with endothelial COX-2 inhibitors (e.g., rofecoxib, celecoxib and high dose aspirin).	Quinapril	53-62	kininogen 1	Homo sapiens	123-133	
12022543-7	2002	RESULTS: Quinapril-treated animals required less cardioversions for ventricular arrhythmias (1.58 +/- 0.40 vs 2.77 +/- 0.22; p < 0.05), had higher wall motion scores assessed by two-dimensional echocardiography (4 = normal to -1 = dyskinesia; 2.11 +/- 0.10 vs 1.50 +/- 0.07; p < 0.05), more complete coronary artery endothelial relaxation to bradykinin (45% +/- 3% vs 7% +/- 4%; p < 0.005), and lower infarct size (24.0% +/- 3.0% vs 40.0% +/- 1.7%; p < 0.0001).	Quinapril	9-18	kininogen 1	Homo sapiens	348-358	
11208485-12	2001	"Tissue type" ACE-Is, e.g. quinapril or perindopril acted through accumulation of endogenous Bk.	Quinapril	27-36	kininogen 1	Homo sapiens	93-95	
11691515-7	2001	Bradykinin-induced release of active t-PA was more than doubled during treatment with quinapril in comparison to placebo or losartan (two-way ANOVA: p < 0.003 for treatment group, p < 0.001 for t-PA response and p = ns for interaction), whereas the substance P response was unaffected.	Quinapril	86-95	kininogen 1	Homo sapiens	0-10