PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
8113980-8	1994	Hexamethonium and atropine abolished tonic VIP output, leaving intact motility responses to PL017 and DPDPE.	Hexamethonium	0-13	vasoactive intestinal peptide	Canis lupus familiaris	43-46	
8304456-8	1994	Atropine reduced and hexamethonium nearly abolished VIP output.	Hexamethonium	21-34	vasoactive intestinal peptide	Canis lupus familiaris	52-55	
8134298-4	1993	A combination of atropine and hexamethonium eliminated the PYY-induced decrement in VIP output and left motor excitation unchanged.	Hexamethonium	30-43	vasoactive intestinal peptide	Canis lupus familiaris	84-87	
2475029-3	1989	VIP release was markedly reduced by tetrodotoxin, perfusion with Ca-free medium, or by hexamethonium but not by atropine.	Hexamethonium	87-100	vasoactive intestinal peptide	Canis lupus familiaris	0-3	
7439634-6	1980	Tetrodotoxin and hexamethonium, but not atropine, inhibited oxytocin-stimulted release of VIP by 80% and 60% respectively.	Hexamethonium	17-30	vasoactive intestinal peptide	Canis lupus familiaris	90-93	
7439634-8	1980	Hexamethonium strongly inhibited neostigmine-stimulated release of VIP.	Hexamethonium	0-13	vasoactive intestinal peptide	Canis lupus familiaris	67-70	
8089398-2	1994	In blood-perfused ileum, ACh (2-200 nmol/min) produced a dose-dependent increase in venous VIP output, which was slightly reduced by hexamethonium (10 nmol/min) and blocked by hexamethonium and atropine (10 nmol/min) in combination.	Hexamethonium	133-146	vasoactive intestinal peptide	Canis lupus familiaris	91-94	
9350974-9	1997	Pancreatic VIP release during VNS was not affected by atropine, whereas ganglionic blockade with hexamethonium nearly abolished the VIP response to VNS (p<0.005 vs control), suggesting that VIP is a postganglionic neurotransmitter in the dog pancreas.	Hexamethonium	97-110	vasoactive intestinal peptide	Canis lupus familiaris	132-135	
9350974-9	1997	Pancreatic VIP release during VNS was not affected by atropine, whereas ganglionic blockade with hexamethonium nearly abolished the VIP response to VNS (p<0.005 vs control), suggesting that VIP is a postganglionic neurotransmitter in the dog pancreas.	Hexamethonium	97-110	vasoactive intestinal peptide	Canis lupus familiaris	132-135	
8859008-14	1996	Hexamethonium or L-NNA (but not atropine) reduced VIP release; CCK8 still enhanced it.	Hexamethonium	0-13	vasoactive intestinal peptide	Canis lupus familiaris	50-53	
7977833-5	1994	The increases in heart rate and lymph VIP output were blocked by hexamethonium.	Hexamethonium	65-78	vasoactive intestinal peptide	Canis lupus familiaris	38-41	
8089398-2	1994	In blood-perfused ileum, ACh (2-200 nmol/min) produced a dose-dependent increase in venous VIP output, which was slightly reduced by hexamethonium (10 nmol/min) and blocked by hexamethonium and atropine (10 nmol/min) in combination.	Hexamethonium	176-189	vasoactive intestinal peptide	Canis lupus familiaris	91-94	
8089398-4	1994	ACh-induced VIP output was decreased slightly by hexamethonium (0.1 mM), and blocked by atropine (0.1 mM) or pirenzepine (0.1 mM).	Hexamethonium	49-62	vasoactive intestinal peptide	Canis lupus familiaris	12-15	
8089398-5	1994	Dimethylphenylpiperazinium (0.1 mM) also caused a small increase in VIP output sensitive to hexamethonium in the ileal tissues containing either the submucous or myenteric plexus.	Hexamethonium	92-105	vasoactive intestinal peptide	Canis lupus familiaris	68-71