PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16220025-12	2006	Suppression of substance P-evoked NO release by Ang II (>70%, n = 6) was reversed by the PKC inhibitor chelerythrine, the DHP amlodipine and nisoldipine and the ACE inhibitor ramiprilat.	ramiprilat	178-188	angiotensinogen	Homo sapiens	48-54	
2438489-2	1986	Ramiprilat (10 mcg/min for 10 min) produced a 71% mean increase in FBF (n = 8; range, 26-130%; p less than 0.001) in vessels preconstricted with ANG I (64-128 pmol/min), with the effect maximal at the end of ramiprilat infusion and subsiding over 30 min.	ramiprilat	0-10	angiotensinogen	Homo sapiens	145-150	
17716647-5	2007	The bradykinin/angiotensin I selectivity ratios calculated from double displacement experiments were: perindoprilat, 1.44; ramiprilat, 1.16; quinaprilat, 1.09; trandolaprilat, 1.08; enalaprilat, 1.00.	ramiprilat	123-133	angiotensinogen	Homo sapiens	15-28	
10397679-8	1999	This effect was inhibited by captopril and ramiprilat, suggesting conversion of angiotensin I to angiotensin II by angiotensin-converting enzyme in SMCs.	ramiprilat	43-53	angiotensinogen	Homo sapiens	80-93	
15530425-3	2004	Therefore, our study concentrates on the effect of the ACE-inhibitor ramiprilat on chemokine release, AngII receptor (ATR) expression, and NF-kappaB activity in monocytes stimulated with AngII.	ramiprilat	69-79	angiotensinogen	Homo sapiens	187-192	
15530425-5	2004	Ramiprilat dose-dependently suppressed AngII-induced upregulation of IL-8 and MCP-1.	ramiprilat	0-10	angiotensinogen	Homo sapiens	39-44	
15530425-6	2004	The suppressive effect of ramiprilat on AngII-induced chemokine production and release was in part caused by downregulation of NF-kappaB, but more by a selective and highly significant reduced expression of AT1 receptors as shown in monocytes and endothelial cells.	ramiprilat	26-36	angiotensinogen	Homo sapiens	40-45	
15530425-8	2004	In addition, ramiprilat downregulated NF-kappaB activity and thereby reduced the AngII-induced release of IL-8 and MCP-1 in monocytes.	ramiprilat	13-23	angiotensinogen	Homo sapiens	81-86	
16088213-4	2005	We analyzed the effect of the ACE inhibitor ramiprilat on AngII-dependent cell adhesion molecule (CAM) expression and adhesion of monocytic THP-1 cells to endothelial cells.	ramiprilat	44-54	angiotensinogen	Homo sapiens	58-63	
16088213-7	2005	Ramiprilat reduced AT 1 expression on endothelial cells and decreased the AngII-induced p65 translocation into the nucleus.	ramiprilat	0-10	angiotensinogen	Homo sapiens	74-79	
16088213-9	2005	Thus, modulation of the local AngII system by ramiprilat may at least in part contribute to the benefits of ACE inhibition in the treatment of atherosclerotic diseases.	ramiprilat	46-56	angiotensinogen	Homo sapiens	30-35	
10397679-8	1999	This effect was inhibited by captopril and ramiprilat, suggesting conversion of angiotensin I to angiotensin II by angiotensin-converting enzyme in SMCs.	ramiprilat	43-53	angiotensinogen	Homo sapiens	97-111	
1650862-4	1991	While ramiprilat itself induced an increase of basal [Ca2+]i, the Ca(2+)-mobilizing effect of angiotensin II (AII) was blunted in the presence of the ACE inhibitor (659 +/- 38 nM vs 360 +/- 45 nM, p less than .001).	ramiprilat	6-16	angiotensinogen	Homo sapiens	94-108	
1650862-9	1991	Ramiprilat-induced contraction of cultured smooth muscle cells may not be relevant in vivo, but the increase of basal [Ca2+]i by ramiprilat may reflect a "reset" of the cellular Ca(2+)-mobilizing mechanism or a depletion of cellular Ca2+ stores and may thus explain the attenuation of the Ca(2+)-mobilizing effect of AII.	ramiprilat	129-139	angiotensinogen	Homo sapiens	317-320