PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10781015-8	2000	Relaxations to thrombin, SFLLRN, trypsin and SLIGRL were significantly inhibited (P<0.05) to similar extents by the nitric oxide (NO) synthase inhibitor N(G)-nitro-L-arginine (L-NOARG; 100 microM) and the NO scavenger oxyhaemoglobin (20 microM), both separately and in combination.	Nitroarginine	156-177	coagulation factor II, thrombin	Homo sapiens	15-23	
12009388-4	2002	RESULTS: Renal arteries responded to thrombin with relaxation, which was inhibited by N(G)-nitro-L-arginine or indomethacin and reversed to contractions by the combination.	Nitroarginine	86-107	coagulation factor II, thrombin	Homo sapiens	37-45	
11139441-7	2000	When the thrombin-induced contraction was inhibited by ONO-3708, either pretreatment with N(omega)-nitro-L-arginine methylester (L-NAME) or an increase in the amount of external K(+) to 40 mM did not abolish thrombin-induced relaxation during phenylephrine-induced sustained contraction.	Nitroarginine	90-115	coagulation factor II, thrombin	Homo sapiens	9-17	
10781015-10	2000	In the presence of the L-type voltage-operated calcium channel (L-VOCC) inhibitor nifedipine (0.3 microM), K(+) (67 mM) abolished the L-NOARG-resistant relaxations to thrombin, SFLLRN, trypsin and SLIGRL.	Nitroarginine	134-141	coagulation factor II, thrombin	Homo sapiens	167-175	
10781015-12	2000	Furthermore, L-NOARG-resistant relaxations to thrombin were abolished by nifedipine, whereas relaxations to SFLLRN, trypsin or SLIGRL were not further inhibited by combined treatment with nifedipine and L-NOARG, than they were with L-NOARG treatment alone.	Nitroarginine	13-20	coagulation factor II, thrombin	Homo sapiens	46-54	
10781015-14	2000	Similar selective inhibition of the L-NOARG-resistant relaxation to thrombin, but not SFLLRN, occurred with verapamil (1 microM) and diltiazem (3 microM).	Nitroarginine	36-43	coagulation factor II, thrombin	Homo sapiens	68-76	
9686762-9	1998	The thrombin-mediated increase in putrescine production was reversed by N(G)-methyl-L-arginine, a competitive inhibitor of cationic amino acid transport, or by alpha-difluoromethylornithine (DFMO), an ODC inhibitor.	Nitroarginine	72-94	coagulation factor II, thrombin	Homo sapiens	4-12	
7534807-3	1995	N omega-nitro-L-arginine, an inhibitor of NO synthase, potentiated thrombin-induced aggregation of washed human platelets, whereas L-arginine inhibited it.	Nitroarginine	0-24	coagulation factor II, thrombin	Homo sapiens	67-75	
8357951-5	1993	The production of nitrite evoked by equieffective concentrations of interleukin-1 beta in the presence and absence of eicosapentaenoic acid were inhibited to a similar extent by nitro L-arginine (an inhibitor of nitric oxide synthase), transforming growth factor beta 1, platelet-derived growth factorAB and thrombin.	Nitroarginine	178-194	coagulation factor II, thrombin	Homo sapiens	308-316	
1501139-8	1992	Nitro-L-arginine-resistant relaxations were evoked by several agents (A23187, thrombin and UK 14304) in addition to bradykinin.	Nitroarginine	0-16	coagulation factor II, thrombin	Homo sapiens	78-86	
1501139-11	1992	Thrombin caused more transient relaxations and hyperpolarizations than bradykinin in the presence of nitro-L-arginine.	Nitroarginine	101-117	coagulation factor II, thrombin	Homo sapiens	0-8	
8139697-7	1994	This is probably due to the release of EDRF from endothelial cells since blockade of EDRF synthesis by NG-nitro-L-arginine augmented the thrombin-induced contractions in arteries with intact endothelium.	Nitroarginine	103-122	coagulation factor II, thrombin	Homo sapiens	137-145	
8238588-2	1993	In rings of coronary arteries and saphenous veins contracted submaximally with prostaglandin F2 alpha or U46619, alpha-thrombin (0.1-10 nM) caused relaxations that were abolished by treatment with N omega-nitro-L-arginine (L-NNA) or removal of the endothelium, indicating that the relaxations were mediated by endothelium-derived nitric oxide.	Nitroarginine	197-221	coagulation factor II, thrombin	Homo sapiens	119-127	
8238588-2	1993	In rings of coronary arteries and saphenous veins contracted submaximally with prostaglandin F2 alpha or U46619, alpha-thrombin (0.1-10 nM) caused relaxations that were abolished by treatment with N omega-nitro-L-arginine (L-NNA) or removal of the endothelium, indicating that the relaxations were mediated by endothelium-derived nitric oxide.	Nitroarginine	223-228	coagulation factor II, thrombin	Homo sapiens	119-127