PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24697908-7	2014	ET-1 antagonized neural nitric oxide (NO)-mediated relaxant responses in LZR arteries, antagonizing relaxations induced by the NO donor S-nitroso-N-acetylpenicillamine to a larger extent in arteries from OZRs.	S-Nitroso-N-Acetylpenicillamine	136-167	endothelin 1	Homo sapiens	0-4	
17644565-4	2007	Treatment of A-10 VSMCs with S-nitroso-N-acetylpenicillamine (SNAP) or sodium nitroprusside (SNP), two NO donors, attenuated the ET-1-enhanced phosphorylation of several key components of growth-promoting and hypertrophic signaling pathways such as ERK1/2, PKB, and Pyk2.	S-Nitroso-N-Acetylpenicillamine	29-60	endothelin 1	Homo sapiens	129-133	
17644565-4	2007	Treatment of A-10 VSMCs with S-nitroso-N-acetylpenicillamine (SNAP) or sodium nitroprusside (SNP), two NO donors, attenuated the ET-1-enhanced phosphorylation of several key components of growth-promoting and hypertrophic signaling pathways such as ERK1/2, PKB, and Pyk2.	S-Nitroso-N-Acetylpenicillamine	62-66	endothelin 1	Homo sapiens	129-133	
8729059-5	1996	Higher concentrations of ET-1 (0.5 and 5 nM) produced a direct elevation in LVEDP which was enhanced by L-NAME and totally blocked by the NO donor S-nitrosoacetylpenicillamine (SNAP, 10 microM) although responses to 5 nM ET-1 were highly variable with no significant differences between treatment groups.	S-Nitroso-N-Acetylpenicillamine	147-175	endothelin 1	Homo sapiens	25-29	
11738101-7	2001	Stimulation of HSCs with S-nitroso-N-acetyl-penicillamine (SNAP), a nitric oxide (NO)-donor, increased the opening of BK(Ca) channels and reduced the effects of endothelin-1.	S-Nitroso-N-Acetylpenicillamine	25-57	endothelin 1	Homo sapiens	161-173	
11738101-7	2001	Stimulation of HSCs with S-nitroso-N-acetyl-penicillamine (SNAP), a nitric oxide (NO)-donor, increased the opening of BK(Ca) channels and reduced the effects of endothelin-1.	S-Nitroso-N-Acetylpenicillamine	59-63	endothelin 1	Homo sapiens	161-173	
11078363-2	2000	Our aim was to compare the ability of the nitric oxide donors (NO-donors) 3-morpholinylsydnonimine (SIN-1) and S-nitroso-N-acetylpenicillamine (SNAP) with the novel nitric oxide donors (NONOates) diethylamine NONOate (DEA/NO), and diethylenetriamine NONOate (DETA/NO) in order to physiologically antagonize ET-1-mediated constriction of human internal mammary arteries (IMA) in vitro.	S-Nitroso-N-Acetylpenicillamine	144-148	endothelin 1	Homo sapiens	307-311	
10993771-5	2000	Sodium nitroprusside and S-nitroso-N-acetyl penicillamine significantly (P > 0.001) decreased ANG II and ET-1 secretion, whereas N(omega)-nitro-L-arginine-methyl ester enhanced it.	S-Nitroso-N-Acetylpenicillamine	25-57	endothelin 1	Homo sapiens	108-112	
8729059-5	1996	Higher concentrations of ET-1 (0.5 and 5 nM) produced a direct elevation in LVEDP which was enhanced by L-NAME and totally blocked by the NO donor S-nitrosoacetylpenicillamine (SNAP, 10 microM) although responses to 5 nM ET-1 were highly variable with no significant differences between treatment groups.	S-Nitroso-N-Acetylpenicillamine	177-181	endothelin 1	Homo sapiens	25-29	
8729059-5	1996	Higher concentrations of ET-1 (0.5 and 5 nM) produced a direct elevation in LVEDP which was enhanced by L-NAME and totally blocked by the NO donor S-nitrosoacetylpenicillamine (SNAP, 10 microM) although responses to 5 nM ET-1 were highly variable with no significant differences between treatment groups.	S-Nitroso-N-Acetylpenicillamine	177-181	endothelin 1	Homo sapiens	221-225