PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
28496430-11	2017	Both nicotine and carbachol induced intracellular Ca2+ transients in trigeminal neurons partially overlapping with expression of capsaicin-sensitive TRPV1 receptors.	Nicotine	5-13	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	149-154	
26881175-7	2016	Nicotine also inhibited toxin A-induced increased colonic concentrations of the TRPV1 (transient receptor potential vanilloid subtype 1) agonist, leukotriene B4 (LTB4), and release of the proinflammatory neuropeptide, substance P. Pretreatment with nicotine did not protect against direct TRPV1-mediated colitis caused by intraluminal capsaicin.	Nicotine	0-8	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	80-85	
26881175-8	2016	Nicotinic cholinergic receptors tonically protect the colon against inflammation and nicotine inhibits toxin A colitis but not toxin A ileitis in rats in part by inhibition of toxin A-induced activation of TRPV1 by endogenous TRPV1 agonists such as LTB4.	Nicotine	85-93	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	206-211	
26881175-7	2016	Nicotine also inhibited toxin A-induced increased colonic concentrations of the TRPV1 (transient receptor potential vanilloid subtype 1) agonist, leukotriene B4 (LTB4), and release of the proinflammatory neuropeptide, substance P. Pretreatment with nicotine did not protect against direct TRPV1-mediated colitis caused by intraluminal capsaicin.	Nicotine	0-8	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	87-135	
26881175-7	2016	Nicotine also inhibited toxin A-induced increased colonic concentrations of the TRPV1 (transient receptor potential vanilloid subtype 1) agonist, leukotriene B4 (LTB4), and release of the proinflammatory neuropeptide, substance P. Pretreatment with nicotine did not protect against direct TRPV1-mediated colitis caused by intraluminal capsaicin.	Nicotine	0-8	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	289-294	
23926288-1	2013	High concentrations of nicotine, as in the saliva of oral tobacco consumers or in smoking cessation aids, have been shown to sensitize/activate recombinant transient receptor potential vanilloid type 1 (rTRPV1) and mouse TRPA1 (mTRPA1) channels.	Nicotine	23-31	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	203-209	
23926288-4	2013	The nicotine response at 20 mM was strongly pHe-dependent, - five times greater at pH 9.0 than 7.4, indicating that intracellular permeation of the (uncharged) alkaloid was required to reach the TRPV1/A1 binding sites.	Nicotine	4-12	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	195-200	
25117291-1	2014	BACKGROUND AND PURPOSE: Previous studies have demonstrated that nicotine releases protons from adrenergic nerves via stimulation of nicotinic ACh receptors and activates transient receptor potential vanilloid-1 (TRPV1) receptors located on calcitonin gene-related peptide (CGRP)-containing (CGRPergic) vasodilator nerves, resulting in vasodilatation.	Nicotine	64-72	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	170-210	
25117291-1	2014	BACKGROUND AND PURPOSE: Previous studies have demonstrated that nicotine releases protons from adrenergic nerves via stimulation of nicotinic ACh receptors and activates transient receptor potential vanilloid-1 (TRPV1) receptors located on calcitonin gene-related peptide (CGRP)-containing (CGRPergic) vasodilator nerves, resulting in vasodilatation.	Nicotine	64-72	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	212-217	
19483072-1	2009	Nicotine stimulates presynaptic nicotinic acetylcholine receptors in perivascular adrenergic nerves and releases unknown transmitter(s) that activate transient receptor potential vanilloid-1 (TRPV1) located on calcitonin gene-related peptide (CGRP)-containing (CGRPergic) nerves, resulting in vasodilation.	Nicotine	0-8	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	192-197	
19483072-1	2009	Nicotine stimulates presynaptic nicotinic acetylcholine receptors in perivascular adrenergic nerves and releases unknown transmitter(s) that activate transient receptor potential vanilloid-1 (TRPV1) located on calcitonin gene-related peptide (CGRP)-containing (CGRPergic) nerves, resulting in vasodilation.	Nicotine	0-8	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	150-190	
19483072-5	2009	Capsazepine (TRPV1 antagonist) blunted nicotine-induced vasodilation, but had no effect on the reduction of pH.	Nicotine	39-47	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	13-18	
19483072-12	2009	These results indicate that nicotine initially stimulates adrenergic nerves via nicotinic alpha(3)beta(4)-receptors to release protons and thereby induces CGRPergic nerve-mediated vasodilation via TRPV1.	Nicotine	28-36	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	197-202	
15249421-5	2004	Capsazepine (vanilloid receptor-1 antagonist; 1-10 microm) and ruthenium red (inhibitor of vanilloid response; 1-30 microm) concentration-dependently inhibited the nicotine-induced vasodilation without affecting the vasodilator response to exogenous CGRP.	Nicotine	164-172	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	13-33	
15249421-10	2004	These results suggest that nicotine acts on presynaptic nicotinic receptors to release adrenergic neurotransmitter(s) or related substance(s), which then stimulate vanilloid receptor-1 on CGRPergic nerves, resulting in CGRP release and vasodilation.	Nicotine	27-35	transient receptor potential cation channel, subfamily V, member 1	Rattus norvegicus	164-184