PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2415954-3 1985 Vasoactive intestinal peptide (VIP) increases cellular cAMP levels in human thyroid cultures and its effect is additive to increases produced by norepinephrine (NE) and isoproterenol (ISO). Norepinephrine 145-159 vasoactive intestinal peptide Homo sapiens 31-34 22660994-6 2012 Plasma levels of chromogranin A, calcitonin, parathormone, basal renin and most prominently VIP were increased in line with a increased 24 hour urinary secretion of noradrenaline, dopamine, normetanephrine and vanillymandelic acid. Norepinephrine 165-178 vasoactive intestinal peptide Homo sapiens 92-95 7538196-2 1995 In the present study, we show that VIP (5-200 nM) treatment increased the intracellular calcium concentration ([Ca2+]i) in 64% of isolated individual pinealocytes; in comparison, norepinephrine (NE) elevated [Ca2+]i in 93% of the cells and produced more robust responses. Norepinephrine 179-193 vasoactive intestinal peptide Homo sapiens 35-38 3711722-9 1986 Myocardial catecholamines were also determined in 14 subjects; a weak correlation (r = 0.57, P less than 0.05) between the tissue concentrations of VIP and norepinephrine was noted. Norepinephrine 156-170 vasoactive intestinal peptide Homo sapiens 148-151 3534807-6 1986 At 6 hours of incubation, VIP stimulated total catecholamine release from fetal adrenomedullary cells in a dose-dependent manner at concentrations ranging from 10(-8) to 10(-4) M. The release of norepinephrine and epinephrine, but not dopamine, was significantly enhanced. Norepinephrine 195-209 vasoactive intestinal peptide Homo sapiens 26-29 11121793-15 2001 In this regard, endogenously released or exogenous VIP can significantly increase the heart rate and has a more potent effect on heart rate than does norepinephrine. Norepinephrine 150-164 vasoactive intestinal peptide Homo sapiens 51-54 7990977-4 1994 Coinfusion of noradrenaline with a weakly venodilating, constant dose of VIP (93.2 pmol/min) caused a 0.5-fold decrease in the sensitivity for noradrenaline. Norepinephrine 14-27 vasoactive intestinal peptide Homo sapiens 73-76 7990977-4 1994 Coinfusion of noradrenaline with a weakly venodilating, constant dose of VIP (93.2 pmol/min) caused a 0.5-fold decrease in the sensitivity for noradrenaline. Norepinephrine 143-156 vasoactive intestinal peptide Homo sapiens 73-76 2200184-2 1990 VIP receptors are coupled to cAMP-generating systems that are amplified by various neurotransmitters such as noradrenaline, histamine and GABA. Norepinephrine 109-122 vasoactive intestinal peptide Homo sapiens 0-3 2576679-5 1989 Here, VIP provokes the excitation, vasodilatation and together with noradrenaline participates in the regulation of cortical energy metabolism. Norepinephrine 68-81 vasoactive intestinal peptide Homo sapiens 6-9 2546435-7 1989 Norepinephrine inhibits VIP-stimulated changes in Isc as well as the basal Isc. Norepinephrine 0-14 vasoactive intestinal peptide Homo sapiens 24-27 3250182-5 1988 In vessels precontracted by noradrenalin 10(-5) M, VIP 10(-8) - 10(-6) M and PHM 10(-8) - 10(-6) M induced similar, concentration-dependent relaxation with a maximum effect of 73.2 +/- 12.7% relaxation for VIP 10(-6) M and 79.6 +/- 11.8% for PHM 10(-6) M, as compared to 10.7 +/- 3.1% decrease in tension for control preparations treated with solvent (mean +/- SE, n = 6). Norepinephrine 28-40 vasoactive intestinal peptide Homo sapiens 51-54 2891636-6 1987 Since there are no major fluctuations in the water content of the tubal tissues in the three phases, the observed changes in VIP levels represent real fluctuations at the neural level in a manner similar to that previously shown for the neurotransmitter norepinephrine. Norepinephrine 254-268 vasoactive intestinal peptide Homo sapiens 125-128 2867688-2 1986 The modulation of cortical VIP release by several neurotransmitters [gamma-aminobutyric acid (GABA), opioids, norepinephrine, acetylcholine, and glutamate] normally present in the cerebral cortex was studied by administering respective agonists and antagonists for their receptors. Norepinephrine 110-124 vasoactive intestinal peptide Homo sapiens 27-30 2875443-9 1986 Furthermore, VIP interacts synergistically with norepinephrine to stimulate cAMP formation and to inhibit the firing rate of spontaneously active identified cortical neurons. Norepinephrine 48-62 vasoactive intestinal peptide Homo sapiens 13-16 24108336-4 2013 Several purines and peptides have been postulated as neurotransmitters of this system, and some of them coexist with the acetylcholine or norepinephrine; for example, vasoactive intestinal peptide (VIP) on cholinergic nerves and neuropeptide Y in the adrenergic nerves. Norepinephrine 138-152 vasoactive intestinal peptide Homo sapiens 167-196 24108336-4 2013 Several purines and peptides have been postulated as neurotransmitters of this system, and some of them coexist with the acetylcholine or norepinephrine; for example, vasoactive intestinal peptide (VIP) on cholinergic nerves and neuropeptide Y in the adrenergic nerves. Norepinephrine 138-152 vasoactive intestinal peptide Homo sapiens 198-201 2984004-7 1985 When tested on intact cells, epinephrine, norepinephrine and clonidine were found to counteract, in a dose-dependent manner, the increase of cyclic AMP triggered by vasoactive intestinal peptide (VIP). Norepinephrine 42-56 vasoactive intestinal peptide Homo sapiens 196-199 2984004-9 1985 The physiological amines were the most efficient agonists: both epinephrine and norepinephrine inhibited VIP-induced cyclic AMP accumulation by 50-55% with KD values of 50 nM and 300 nM respectively. Norepinephrine 80-94 vasoactive intestinal peptide Homo sapiens 105-108 6400363-2 1984 They can serve as cotransmitters in the autonomic nervous system; for example, vasoactive intestinal peptide (VIP) is released with acetylcholine and neuropeptide Y with norepinephrine from postganglionic neurons. Norepinephrine 170-184 vasoactive intestinal peptide Homo sapiens 110-113