PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 2536238-4 1989 Perfusion with tachykinins (substance P and substance K), vasoactive intestinal peptide, forskolin, or serotonin also significantly increased the release of [3H]ACh. Acetylcholine 161-164 tachykinin precursor 1 Homo sapiens 28-55 2472601-0 1989 Substance P, like acetylcholine, augments one type of Ca2+ current in isolated smooth muscle cells. Acetylcholine 18-31 tachykinin precursor 1 Homo sapiens 0-11 2472601-4 1989 Thus, substance P, like acetylcholine, has a dual excitatory action on the smooth muscle cells employed in these studies, enhancing a specific type of Ca2+ current, as demonstrated here, and suppressing a voltage-sensitive K+ conductance, as previously described [Sims, S.M., Walsh, J.V., Jr. & Singer, J.J. (1986) Am. Acetylcholine 24-37 tachykinin precursor 1 Homo sapiens 6-17 2451792-4 1988 The ACh-evoked firing was antagonized by D-tubocurarine (D-TC), atropine (ATR) and SP. Acetylcholine 4-7 tachykinin precursor 1 Homo sapiens 83-85 2462362-8 1988 NKA, NKB, and SP caused a dose-dependent, tetrodotoxin-sensitive increase in [3H]acetylcholine release from strips preincubated with [3H]choline. Acetylcholine 81-94 tachykinin precursor 1 Homo sapiens 0-3 2462362-9 1988 NKA was significantly more potent to release [3H]acetylcholine than either NKB or SP. Acetylcholine 45-62 tachykinin precursor 1 Homo sapiens 0-3 2443476-4 1987 Pretreatment with hemicholinium 3, an acetylcholine synthesis inhibitor, inhibited the contractile response to SP. Acetylcholine 38-51 tachykinin precursor 1 Homo sapiens 111-113 2856543-1 1988 In some animal species substance P and neurokinin A (NKA) cause bronchoconstriction by the release of acetylcholine from postganglionic cholinergic nerve endings. Acetylcholine 102-115 tachykinin precursor 1 Homo sapiens 23-34 2856543-1 1988 In some animal species substance P and neurokinin A (NKA) cause bronchoconstriction by the release of acetylcholine from postganglionic cholinergic nerve endings. Acetylcholine 102-115 tachykinin precursor 1 Homo sapiens 39-51 2856543-1 1988 In some animal species substance P and neurokinin A (NKA) cause bronchoconstriction by the release of acetylcholine from postganglionic cholinergic nerve endings. Acetylcholine 102-115 tachykinin precursor 1 Homo sapiens 53-56 2888665-6 1987 Compared to non-peptide agents, NKA had an affinity 2-3 orders of magnitude greater than acetylcholine and histamine but produced only 75-80% of the maximal effect of acetylcholine. Acetylcholine 167-180 tachykinin precursor 1 Homo sapiens 32-35 3039119-6 1987 ), a putative substance P antagonist, reduced responses to mammalian neurokinins but caused a 2-fold potentiation of acetylcholine-induced salivation. Acetylcholine 117-130 tachykinin precursor 1 Homo sapiens 14-25 2429556-7 1986 These results indicate that substance P suppresses the same outward K+ current affected by ACh. Acetylcholine 91-94 tachykinin precursor 1 Homo sapiens 28-39 2436021-6 1987 In vitro studies showed that NKA was the most potent of the tachykinins as a bronchoconstrictor agent, being several hundred-fold more active than SP, acetylcholine and histamine. Acetylcholine 151-164 tachykinin precursor 1 Homo sapiens 29-32 2432378-4 1987 The amount of ACh released into the bathing medium in response to tetanic stimulation of the phrenic nerve was doubled in presence of sP. Acetylcholine 14-17 tachykinin precursor 1 Homo sapiens 134-136 6198467-8 1984 These in vitro studies suggest a similar role for substance P in vivo: substance P"s protection against nicotinic desensitization may ensure a maintained output of adrenal catecholamines during stress, when the splanchnic nerve releases large amounts of acetylcholine. Acetylcholine 254-267 tachykinin precursor 1 Homo sapiens 71-82 6198467-1 1984 Substance P, a peptide endogenous to the splanchnic nerve, is known to inhibit the acetylcholine-and nicotine-induced release of catecholamines from isolated adrenal chromaffin cells. Acetylcholine 83-96 tachykinin precursor 1 Homo sapiens 0-11 2425310-8 1986 These results suggest that SP presynaptically facilitates the neuromuscular transmission, increasing the evoked release of ACh from motor nerve terminals. Acetylcholine 123-126 tachykinin precursor 1 Homo sapiens 27-29 2414777-2 1985 Substance P and the recently discovered neurokinins elicit contraction of the ileum both directly through action on a muscle cell receptor and indirectly through stimulation of a neuronal receptor, leading to release of acetylcholine, which causes muscle contraction via muscarinic receptors. Acetylcholine 220-233 tachykinin precursor 1 Homo sapiens 0-11 6201867-0 1984 Substance P modulation of acetylcholine-induced currents in embryonic chicken sympathetic and ciliary ganglion neurons. Acetylcholine 26-39 tachykinin precursor 1 Homo sapiens 0-11 6201867-4 1984 This report demonstrates a direct effect of substance P on acetylcholine-induced inward currents in both sympathetic and parasympathetic neurons clamped near resting membrane potential. Acetylcholine 59-72 tachykinin precursor 1 Homo sapiens 44-55 6198467-3 1984 Substance P (10(-5) M) completely protected against desensitization of catecholamine release produced by acetylcholine at 37 degrees C or 23 degrees C and by nicotine at 23 degrees C; substance P also afforded appreciable protection against nicotine-induced desensitization at 37 degrees C. The peptide had no effect on K+-induced desensitization of catecholamine release. Acetylcholine 105-118 tachykinin precursor 1 Homo sapiens 0-11 6191578-0 1983 Does substance P comediate with acetylcholine in nerves of opossum esophageal muscularis mucosa? Acetylcholine 32-45 tachykinin precursor 1 Homo sapiens 5-16 6191578-8 1983 We postulate that acetylcholine and substance P may coexist in and be coreleased from nerves of this muscle and that the acetylcholine release occurs first, causing an initial phasic response and delaying and diminishing the release of substance P. Acetylcholine 121-134 tachykinin precursor 1 Homo sapiens 236-247 6201245-3 1984 Moreover, prior application of substance P strongly depressed the electrical response of the mucosa to acetylcholine. Acetylcholine 103-116 tachykinin precursor 1 Homo sapiens 31-42 6196519-0 1983 Substance P facilitates the release of acetylcholine from motor nerve terminals of frogs. Acetylcholine 39-52 tachykinin precursor 1 Homo sapiens 0-11 7172036-3 1982 Three hypotheses accounting for the localization of acetylcholinesterase within and/or on substantia nigra, pars compacta neurons are presented and evaluated: (a) to catabolize acetylcholine released from afferent cholinergic fibers, (b) to catabolize substance P released from some neostriato-nigral axon terminals, and/or (c) to serve as a communication link with nigral vasculature. Acetylcholine 52-65 tachykinin precursor 1 Homo sapiens 252-263 7352016-7 1980 The reversal potential for substance P is shown to be identical to that obtained in the same cells for acetylcholine (ACh) and adrenaline. Acetylcholine 103-116 tachykinin precursor 1 Homo sapiens 27-38 6191322-5 1981 It is suggested that methionine enkephalin and/or beta-endorphin and Substance P regulate release of acetylcholine or hormones from placental villus. Acetylcholine 101-114 tachykinin precursor 1 Homo sapiens 69-80 7352016-7 1980 The reversal potential for substance P is shown to be identical to that obtained in the same cells for acetylcholine (ACh) and adrenaline. Acetylcholine 118-121 tachykinin precursor 1 Homo sapiens 27-38 15501528-0 2004 Neurokinin-1 receptor antagonism by SR140333: enhanced in vivo ACh in the hippocampus and promnestic post-trial effects. Acetylcholine 63-66 tachykinin precursor 1 Homo sapiens 0-12 95417-0 1979 An investigation of whether septal gamma-aminobutyrate-containing interneurons are involved in the reduction in the turnover rate of acetylcholine elicited by substance P and beta-endorphin in the hippocampus. Acetylcholine 133-146 tachykinin precursor 1 Homo sapiens 159-170 13798429-2 1960 The stimulating action of acetylcholine on the superior cervical ganglion (as judged by the response of the nictitating membrane) was also potentiated by substance P. Acetylcholine 26-39 tachykinin precursor 1 Homo sapiens 154-165 20882546-2 2012 Systemic application of NK(2)-R antagonists block the release of acetylcholine (ACh) in the hippocampus, which is induced by intraseptal administration of the NK(2)-R ligand, neurokinin A (NKA). Acetylcholine 80-83 tachykinin precursor 1 Homo sapiens 189-192 20882546-5 2012 ACh levels in hippocampus and amygdala, but not in frontal cortex were increased after intraseptal injection of either NKA or NKB (0.1, 1, 10 muM). Acetylcholine 0-3 tachykinin precursor 1 Homo sapiens 119-122 21515660-5 2011 Furthermore, [Ca(2+)](i) responses to 1 muM ACh as well as BDNF (30 min) effects on [Ca(2+)](i) regulation were enhanced by prior SP exposure, largely via increased Ca(2+) influx (P < 0.05). Acetylcholine 44-47 tachykinin precursor 1 Homo sapiens 130-132 30186388-11 2018 PPT and DPN inhibited ACh-induced contraction in GSMCs from females. Acetylcholine 22-25 tachykinin precursor 1 Homo sapiens 0-3 20882546-0 2012 Neurokinin2-R in medial septum regulate hippocampal and amygdalar ACh release induced by intraseptal application of neurokinins A and B. Acetylcholine 66-69 tachykinin precursor 1 Homo sapiens 0-11 20882546-0 2012 Neurokinin2-R in medial septum regulate hippocampal and amygdalar ACh release induced by intraseptal application of neurokinins A and B. Acetylcholine 66-69 tachykinin precursor 1 Homo sapiens 116-135 20882546-2 2012 Systemic application of NK(2)-R antagonists block the release of acetylcholine (ACh) in the hippocampus, which is induced by intraseptal administration of the NK(2)-R ligand, neurokinin A (NKA). Acetylcholine 65-78 tachykinin precursor 1 Homo sapiens 175-187 20882546-2 2012 Systemic application of NK(2)-R antagonists block the release of acetylcholine (ACh) in the hippocampus, which is induced by intraseptal administration of the NK(2)-R ligand, neurokinin A (NKA). Acetylcholine 65-78 tachykinin precursor 1 Homo sapiens 189-192 20882546-2 2012 Systemic application of NK(2)-R antagonists block the release of acetylcholine (ACh) in the hippocampus, which is induced by intraseptal administration of the NK(2)-R ligand, neurokinin A (NKA). Acetylcholine 80-83 tachykinin precursor 1 Homo sapiens 175-187 16931551-4 2006 We investigated the effects of different concentrations of calcitonin gene-related peptide (CGRP), vasoactive intestinal peptide (VIP) and substance P (SP) on acetylcholine-induced axon reflex sweating in healthy subjects (total n = 18). Acetylcholine 159-172 tachykinin precursor 1 Homo sapiens 152-154 14698651-6 2003 RESULTS: Acetylcholine, substance P and sodium nitroprusside caused dose-dependent increases in blood flow (P < 0.001) and substance P caused a dose-dependent increase in tissue-type plasminogen activator (t-PA) release (P < 0.001) in all groups. Acetylcholine 9-22 tachykinin precursor 1 Homo sapiens 126-137 9059313-9 1997 NG-Monomethyl-L-arginine caused a mean reduction in basal blood flow of 42-45% (P < 0.001) and significantly inhibited the responses to both substance P (P < 0.001) and acetylcholine (P = 0.05). Acetylcholine 175-188 tachykinin precursor 1 Homo sapiens 144-155 12398158-3 2002 Among several spasmogens, neurokinin A was the most potent with the following order of potency: carbachol, prostaglandin F2alpha and acetylcholine. Acetylcholine 133-146 tachykinin precursor 1 Homo sapiens 26-38 11049731-5 2000 Secondly, SP injection into the ventral pallidum can lead to increases of acetylcholine in frontal cortex and dopamine in nucleus accumbens, suggesting that the hypermnestic, positively reinforcing and anxiolytic effects observed upon basal forebrain injection of SP are mediated by activation of the nucleus accumbens-ventral pallidum circuitry. Acetylcholine 74-87 tachykinin precursor 1 Homo sapiens 10-12 9543242-3 1998 The rank order of potency was neuropeptide gamma > carbachol > neurokinin A > or = [Nle10]neurokinin A-(4-10) > acetylcholine > or = histamine. Acetylcholine 124-137 tachykinin precursor 1 Homo sapiens 99-111 11514282-3 2001 Acetylcholine and potassium, which act directly on smooth muscle cells to increase [Ca(2+)](i), were found to indirectly elevate [Ca(2+)](i) in endothelial cells; in primary cultures of endothelial cells, neither stimulus affected [Ca(2+)](i), yet substance P increased the fluorescence ratio twofold. Acetylcholine 0-13 tachykinin precursor 1 Homo sapiens 248-259 10491292-3 1999 In contrast, adrenaline, acetylcholine, histamine and CGRP induced only low amount of SP from cultured normal human KCs. Acetylcholine 25-38 tachykinin precursor 1 Homo sapiens 86-88 9688607-6 1998 Canine p38 MAPK was found to be expressed in colonic, tracheal, and vascular smooth muscles and underwent increased tyrosine phosphorylation in response to motor neurotransmitters, acetylcholine (ACh) and neurokinin A (NKA), in colonic smooth muscle. Acetylcholine 196-199 tachykinin precursor 1 Homo sapiens 219-222 1377730-5 1992 Also acetylcholine infusion causes a significant release of SP and NKA after infusion of both atropine and phentolamine (to 172 +/- 56% and 232 +/- 69% of basal release, n = 7), an effect that was abolished by hexamethonium infusion. Acetylcholine 5-18 tachykinin precursor 1 Homo sapiens 60-62 7528464-8 1995 A significant correlation was found between the highest blood flow responses with acetylcholine and with substance P (r = 0.58; p < 0.001). Acetylcholine 82-95 tachykinin precursor 1 Homo sapiens 105-116 7515084-9 1994 A significant correlation was found between the maximal blood flow with acetylcholine and that with substance P (r = 0.68, p < 0.004). Acetylcholine 72-85 tachykinin precursor 1 Homo sapiens 100-111 8899060-9 1996 Our results indicate that the physiological contractile responses of the rat duodenum are co-mediated by acetylcholine and tachykinins, for which NK2 receptors seem to be most important. Acetylcholine 105-118 tachykinin precursor 1 Homo sapiens 146-149 7507436-4 1993 In segments where vasospasm was induced by ergonovine and/or acetylcholine, changes in diameter in response to substance P did not differ from those in non-spastic segments; maximal dilation averaged 27.1 +/- 9.5% in the spastic segments and 24.4 +/- 9.6% in the non-spastic segments (expressed as a percent increase over the value before drug administration). Acetylcholine 61-74 tachykinin precursor 1 Homo sapiens 111-122 7684070-4 1993 Substance P increased the apparent affinity of the cholinergic agonists carbamylcholine and acetylcholine at equilibrium. Acetylcholine 92-105 tachykinin precursor 1 Homo sapiens 0-11 7684070-5 1993 The effect of substance P on the equilibrium binding of [3H]acetylcholine was examined directly, and the peptide appeared to increase the affinity of the binding of the second molecule of agonist, with no effect on the binding of the first. Acetylcholine 56-73 tachykinin precursor 1 Homo sapiens 14-25 7684296-7 1993 In the absence of phosphoramidon, passive sensitization significantly increased the amplitude of the contractile responses to SP and NKA including that to the maximal concentration given from 50 +/- 5% to 76 +/- 6% (n = 5, P < 0.05) and from 70 +/- 7% to 101 +/- 6% (n = 5, P < 0.05) of the maximal response to acetylcholine, respectively. Acetylcholine 317-330 tachykinin precursor 1 Homo sapiens 126-128 7684296-7 1993 In the absence of phosphoramidon, passive sensitization significantly increased the amplitude of the contractile responses to SP and NKA including that to the maximal concentration given from 50 +/- 5% to 76 +/- 6% (n = 5, P < 0.05) and from 70 +/- 7% to 101 +/- 6% (n = 5, P < 0.05) of the maximal response to acetylcholine, respectively. Acetylcholine 317-330 tachykinin precursor 1 Homo sapiens 133-136 7684296-10 1993 In the presence of phosphoramidon (10 microM), passive sensitization still increased significantly the amplitude of the contractile responses to SP and NKA including that to the maximal concentration given from 74 +/- 4% to 115 +/- 7% (n = 5, P<0.05) and from 104 +/- 9% to 146 +/- 16% (n = 5, P<0.05)of the maximal response to acetylcholine, respectively. Acetylcholine 334-347 tachykinin precursor 1 Homo sapiens 145-147 7684296-10 1993 In the presence of phosphoramidon (10 microM), passive sensitization still increased significantly the amplitude of the contractile responses to SP and NKA including that to the maximal concentration given from 74 +/- 4% to 115 +/- 7% (n = 5, P<0.05) and from 104 +/- 9% to 146 +/- 16% (n = 5, P<0.05)of the maximal response to acetylcholine, respectively. Acetylcholine 334-347 tachykinin precursor 1 Homo sapiens 152-155 1377730-5 1992 Also acetylcholine infusion causes a significant release of SP and NKA after infusion of both atropine and phentolamine (to 172 +/- 56% and 232 +/- 69% of basal release, n = 7), an effect that was abolished by hexamethonium infusion. Acetylcholine 5-18 tachykinin precursor 1 Homo sapiens 67-70 1371774-2 1992 This study aimed to determine if endothelium-dependent vasodilation evoked with substance P (SP) was altered at the spastic site where vasospasm was induced by acetylcholine (ACH) in patients with variant angina. Acetylcholine 160-173 tachykinin precursor 1 Homo sapiens 80-91 1582228-3 1992 In the freshly isolated coronary arteries, addition of prostaglandin F2 alpha, endothelin (ET-1), or acetylcholine consistently produced a dose-dependent contraction, reaching a maximum contractile force of 9.6 +/- 0.7, 4.5 +/- 0.5, and 3.1 +/- 0.5 g (M +/- SEM), respectively, while histamine, thrombin and substance P consistently produced an endothelium-dependent relaxation (EDR) with a maximum of -89 +/- 2.8, -85 +/- 5.0, and -72 +/- 3.5%, respectively. Acetylcholine 101-114 tachykinin precursor 1 Homo sapiens 308-319 1371774-2 1992 This study aimed to determine if endothelium-dependent vasodilation evoked with substance P (SP) was altered at the spastic site where vasospasm was induced by acetylcholine (ACH) in patients with variant angina. Acetylcholine 160-173 tachykinin precursor 1 Homo sapiens 93-95 1371774-2 1992 This study aimed to determine if endothelium-dependent vasodilation evoked with substance P (SP) was altered at the spastic site where vasospasm was induced by acetylcholine (ACH) in patients with variant angina. Acetylcholine 175-178 tachykinin precursor 1 Homo sapiens 80-91 1371774-2 1992 This study aimed to determine if endothelium-dependent vasodilation evoked with substance P (SP) was altered at the spastic site where vasospasm was induced by acetylcholine (ACH) in patients with variant angina. Acetylcholine 175-178 tachykinin precursor 1 Homo sapiens 93-95 1707710-18 1990 The response to activation of NK3-receptors is totally neurogenic and partially mediated by endogenous acetylcholine, the response to activation of NK1-receptors is partly neurogenic and largely myogenic and the response to activation of NK2-receptors is totally myogenic. Acetylcholine 103-116 tachykinin precursor 1 Homo sapiens 238-241 2032388-4 1991 In human small coronary arteries taken from the atrial appendage, however, acetylcholine caused concentration-dependent contraction with a functionally intact endothelium as shown by the relaxation in response to substance P, another stimulant of EDRF release. Acetylcholine 75-88 tachykinin precursor 1 Homo sapiens 213-224 1690566-1 1990 Substance P (SP) is present in avian sympathetic ganglia and accelerates the decay rate of acetylcholine (ACh)-evoked macroscopic currents in sympathetic neurons. Acetylcholine 91-104 tachykinin precursor 1 Homo sapiens 0-11 1690566-1 1990 Substance P (SP) is present in avian sympathetic ganglia and accelerates the decay rate of acetylcholine (ACh)-evoked macroscopic currents in sympathetic neurons. Acetylcholine 91-104 tachykinin precursor 1 Homo sapiens 13-15 1690566-1 1990 Substance P (SP) is present in avian sympathetic ganglia and accelerates the decay rate of acetylcholine (ACh)-evoked macroscopic currents in sympathetic neurons. Acetylcholine 106-109 tachykinin precursor 1 Homo sapiens 0-11 1690566-1 1990 Substance P (SP) is present in avian sympathetic ganglia and accelerates the decay rate of acetylcholine (ACh)-evoked macroscopic currents in sympathetic neurons. Acetylcholine 106-109 tachykinin precursor 1 Homo sapiens 13-15 1690566-2 1990 We demonstrate here that SP modulates ACh-elicited single channels in a manner consistent with an enhancement of ACh receptor (AChR) desensitization. Acetylcholine 38-41 tachykinin precursor 1 Homo sapiens 25-27 1690566-4 1990 SP specifically decreases the net ACh-activated single-channel current across the patch membrane by decreasing both channel opening frequency and mean open time kinetics. Acetylcholine 34-37 tachykinin precursor 1 Homo sapiens 0-2