PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 3902630-0 1985 Effect of insulin on placental acetylcholine in normal and diabetic pregnancy. Acetylcholine 31-44 insulin Homo sapiens 10-17 365654-2 1979 Lanthanum inhibits insulin secretion stimulated by glucose and by acetylcholine to basal levels. Acetylcholine 66-79 insulin Homo sapiens 19-26 6108678-5 1980 Similarly, the secretion of insulin, glucagon, pancreatic polypeptide, and somatostatin in response to arginine and acetylcholine was unchanged; arginine stimulated the secretion of all four peptides, whereas acetylcholine stimulated the secretion of insulin and pancreatic polypeptide and inhibited glucagon and somatostatin secretion. Acetylcholine 116-129 insulin Homo sapiens 28-35 790976-1 1976 An in vitro perifusion system utilizing collagen-medium calcium on the dynamics of insulin release as induced by acetylcholine (ACh) stimulation (in the presence of glucose, 2.4 mM) and as modified by prior perfusion of islets in epinephrine. Acetylcholine 113-126 insulin Homo sapiens 83-90 790976-1 1976 An in vitro perifusion system utilizing collagen-medium calcium on the dynamics of insulin release as induced by acetylcholine (ACh) stimulation (in the presence of glucose, 2.4 mM) and as modified by prior perfusion of islets in epinephrine. Acetylcholine 128-131 insulin Homo sapiens 83-90 790976-2 1976 Continuous challenge with ACh produces a biphasic insulin release response, both phases of which are reduced when the medium calcium concentration is reduced during stimulation; when the calcium content is reduced during an initial perifusion period of 30 min and then replaced during subsequent stimulation only the first phase of the response to ACh is affected; perifusion with epinephrine prior to stimulation with ACh produces enhancement of both phases of ACh-induced insulin release when calcium in both media is normal. Acetylcholine 26-29 insulin Homo sapiens 50-57 790976-2 1976 Continuous challenge with ACh produces a biphasic insulin release response, both phases of which are reduced when the medium calcium concentration is reduced during stimulation; when the calcium content is reduced during an initial perifusion period of 30 min and then replaced during subsequent stimulation only the first phase of the response to ACh is affected; perifusion with epinephrine prior to stimulation with ACh produces enhancement of both phases of ACh-induced insulin release when calcium in both media is normal. Acetylcholine 348-351 insulin Homo sapiens 50-57 790976-2 1976 Continuous challenge with ACh produces a biphasic insulin release response, both phases of which are reduced when the medium calcium concentration is reduced during stimulation; when the calcium content is reduced during an initial perifusion period of 30 min and then replaced during subsequent stimulation only the first phase of the response to ACh is affected; perifusion with epinephrine prior to stimulation with ACh produces enhancement of both phases of ACh-induced insulin release when calcium in both media is normal. Acetylcholine 348-351 insulin Homo sapiens 50-57 790976-2 1976 Continuous challenge with ACh produces a biphasic insulin release response, both phases of which are reduced when the medium calcium concentration is reduced during stimulation; when the calcium content is reduced during an initial perifusion period of 30 min and then replaced during subsequent stimulation only the first phase of the response to ACh is affected; perifusion with epinephrine prior to stimulation with ACh produces enhancement of both phases of ACh-induced insulin release when calcium in both media is normal. Acetylcholine 348-351 insulin Homo sapiens 50-57 790976-3 1976 However,.when this experiment is repeated utilizing a medium with low calcium content during the period of exposure to epinephrine the priming effect of epinephrine on the subsequent insulin response to ACh is abolished (in fact, reversed). Acetylcholine 203-206 insulin Homo sapiens 183-190 30873601-1 2019 Pancreatic acinar cells synthesize and secrete about 20 digestive enzymes and ancillary proteins with the processes that match the supply of these enzymes to their need in digestion being regulated by a number of hormones (CCK, secretin and insulin), neurotransmitters (acetylcholine and VIP) and growth factors (EGF and IGF). Acetylcholine 270-283 insulin Homo sapiens 241-248 4834288-0 1974 Extracellular calcium and acetylcholine-stimualted insulin secretion. Acetylcholine 26-39 insulin Homo sapiens 51-58 26904947-4 2016 We show that acetylcholine-mediated insulin secretion requires nicotinic signaling and that nicotinic receptor expression is positively correlated with insulin secretion and glycemic control in human donor islets. Acetylcholine 13-26 insulin Homo sapiens 36-43 30328320-0 2018 Impact of Insulin Resistance on Acetylcholine-Induced Coronary Artery Spasm in Non-Diabetic Patients. Acetylcholine 32-45 insulin Homo sapiens 10-17 27138453-7 2016 On the other hand, the regulatory properties of phospholipase C isoforms determine the interaction of glucose, acetylcholine and free fatty acids (FFA) (that act through the FFA receptors) on insulin secretion. Acetylcholine 111-124 insulin Homo sapiens 192-199 21800096-9 2011 Vascular dysfunction was evident in insulin resistance as increased vascular contractility to PE and decreased relaxation to ACh, whereas PTX protected against this dysfunction. Acetylcholine 125-128 insulin Homo sapiens 36-43 25089090-4 2014 Insulin sensitivity was assessed by homeostasis model assessment (HOMA) and endothelial function by forearm vasodilation (strain-gage venous plethysmography) to intra-arterial acetylcholine (ACH) with sodium nitroprusside (NIP) as a NO-independent control. Acetylcholine 176-189 insulin Homo sapiens 0-7 25089090-4 2014 Insulin sensitivity was assessed by homeostasis model assessment (HOMA) and endothelial function by forearm vasodilation (strain-gage venous plethysmography) to intra-arterial acetylcholine (ACH) with sodium nitroprusside (NIP) as a NO-independent control. Acetylcholine 191-194 insulin Homo sapiens 0-7 22411248-5 2012 Insulin may have a neuroprotective role and may have some impact on acetylcholine (ACh) synthesis. Acetylcholine 68-81 insulin Homo sapiens 0-7 22411248-5 2012 Insulin may have a neuroprotective role and may have some impact on acetylcholine (ACh) synthesis. Acetylcholine 83-86 insulin Homo sapiens 0-7 26308735-7 2015 RESULTS: The pathway analysis of the GWAS dataset identified significant pathways related to oocyte meiosis and the regulation of insulin secretion by acetylcholine and free fatty acids (all nominal gene-set enrichment analysis (GSEA) P-values < 0.05). Acetylcholine 151-164 insulin Homo sapiens 130-137 24658304-5 2014 We found that endogenous acetylcholine not only stimulates the insulin-secreting beta-cell via the muscarinic acetylcholine receptors M3 and M5, but also the somatostatin-secreting delta-cell via M1 receptors. Acetylcholine 25-38 insulin Homo sapiens 63-70 24460367-0 2014 Insulin resistance is associated with lower acetylcholine-induced microvascular reactivity in nondiabetic women. Acetylcholine 44-57 insulin Homo sapiens 0-7 20923961-6 2010 In control subjects, significant potentiation of the vasodilator responses to acetylcholine, nitroprusside, and verapamil was observed after insulin infusion (all P < 0.05). Acetylcholine 78-91 insulin Homo sapiens 141-148 20023776-9 2009 Furthermore, stimulation of insulin secretion by high glucose or acetylcholine administration to a levitated drop containing insulin-producing beta-cells resulted in inhibition of isoprenaline-induced lipolysis in adipocytes present in the same drop. Acetylcholine 65-78 insulin Homo sapiens 28-35 21063035-2 2010 Ethanol impairs neuronal survival and function by two major mechanisms: 1) it inhibits insulin signaling required for viability, metabolism, synapse formation, and acetylcholine production; and 2) it functions as a neurotoxicant, causing oxidative stress, DNA damage and mitochondrial dysfunction. Acetylcholine 164-177 insulin Homo sapiens 87-94 20023776-9 2009 Furthermore, stimulation of insulin secretion by high glucose or acetylcholine administration to a levitated drop containing insulin-producing beta-cells resulted in inhibition of isoprenaline-induced lipolysis in adipocytes present in the same drop. Acetylcholine 65-78 insulin Homo sapiens 125-132 18593766-9 2008 ACh responses during insulin infusion were significantly greater in normal-weight PCOS and controls than in obese PCOS and controls. Acetylcholine 0-3 insulin Homo sapiens 21-28 19090988-4 2008 It is speculated that angiotensin IV may interact with insulin-regulated amino peptidase to enhance neuronal glucose uptake, prevent metabolism of other neuroactive peptides, induce changes in extracellular matrix molecules, or induce release of acetylcholine and/or dopamine. Acetylcholine 246-259 insulin Homo sapiens 55-62 15866056-9 2005 The postprandial microvascular response to Ach was stronger following insulin lispro compared with regular insulin [30 min pp: 26.0 (19.0-49.3) vs. 20.9 (9.7-26.1) AU, P=.0001]. Acetylcholine 43-46 insulin Homo sapiens 70-77 16633080-5 2006 A 60 minute intraarterial infusion of the ET(A) receptor antagonist BQ123 (10 nmol/min) combined with the ET(B) receptor antagonist BQ788 (5 nmol/min) evoked a significant increase in acetylcholine-mediated EDV (P < 0.01) in individuals with insulin resistance. Acetylcholine 184-197 insulin Homo sapiens 245-252 18574072-7 2008 Insulin sensitivity correlated positively to endothelium-dependent vasodilation only in the patient group in both low (beta=0.59; P=0.04) and high (beta=0.53; P=0.04) concentrations of acetylcholine and in a high concentration of sodium nitroprusside (beta=0.0007; P=0.006). Acetylcholine 185-198 insulin Homo sapiens 0-7 18451634-3 2008 The aim of the present study was to evaluate the effects of low- and high-concentration insulin on the concentration-response curves to norepinephrine and acetylcholine in subcutaneous small resistance arteries of hypertensive and diabetic patients. Acetylcholine 155-168 insulin Homo sapiens 88-95 17662981-3 2007 Acute exposure to acetylcholine mimicked insulin action on inactivation of phosphorylase, stimulation of glycogen synthesis and suppression of phosphoenolpyruvate carboxykinase mRNA levels but with lower efficacy and without synergy. Acetylcholine 18-31 insulin Homo sapiens 41-48 17662981-4 2007 Pre-exposure to acetylcholine had a permissive effect on insulin action similar to glucocorticoids and associated with increased glucokinase activity. Acetylcholine 16-29 insulin Homo sapiens 57-64 17662981-5 2007 It is concluded that acetylcholine has a permissive effect on insulin action but cannot fully account for the rapid stimulation of glucose uptake by the portal signal. Acetylcholine 21-34 insulin Homo sapiens 62-69 15866056-9 2005 The postprandial microvascular response to Ach was stronger following insulin lispro compared with regular insulin [30 min pp: 26.0 (19.0-49.3) vs. 20.9 (9.7-26.1) AU, P=.0001]. Acetylcholine 43-46 insulin Homo sapiens 107-114 14747233-16 2004 Coinfusion of exogenous insulin increased ACh response further in the rosiglitazone group. Acetylcholine 42-45 insulin Homo sapiens 24-31 15089786-9 2004 Further, the size of the response to C-peptide correlated well with the size of the response to the endothelium-dependent vasodilatator ACh (r = 0.666, P = 0.001) but not with the size of the response to the endothelium-independent vasodilator SNP (r = 0.345, P > 0.05). Acetylcholine 136-139 insulin Homo sapiens 37-46 15204243-9 2004 Patients had a reduced ACh response but insulin infusion increased the ACh response equally in patients and controls (a mean increase of 74+/-37 vs 57+/-24%, patients vs controls, p=0.12). Acetylcholine 71-74 insulin Homo sapiens 40-47 14656737-1 2004 OBJECTIVE: Human insulin enhances the vasodilatory effect of acetylcholine (ACh), an endothelium-dependent vasodilator, in normal subjects. Acetylcholine 61-74 insulin Homo sapiens 17-24 14656737-1 2004 OBJECTIVE: Human insulin enhances the vasodilatory effect of acetylcholine (ACh), an endothelium-dependent vasodilator, in normal subjects. Acetylcholine 76-79 insulin Homo sapiens 17-24 15772782-0 2005 Insulin resistance relates to acetylcholine-induced microvascular vasoconstriction in a patient with vasospastic angina: potential implication of causalities between hyperinsulinemia and coronary microcirculation failure. Acetylcholine 30-43 insulin Homo sapiens 0-7 15772782-1 2005 Coronary vasomotor response to acetylcholine infusion was studied in a 69-year-old currently smoking man with enhanced insulin response to oral glucose load. Acetylcholine 31-44 insulin Homo sapiens 119-126 15772782-5 2005 This is the first case reported so far suggesting that enhanced insulin response may be associated with acetylcholine-induced microvascular vasoconstriction. Acetylcholine 104-117 insulin Homo sapiens 64-71 15136505-7 2004 Capillary recruitment and acetylcholine-mediated vasodilation were positively correlated with insulin sensitivity (r=0.58, P<0.01 and r=0.55, P<0.01, respectively) and negatively with blood pressure (r=-0.64, P<0.001 and r=-0.42, P<0.05, respectively) in both lean and obese women. Acetylcholine 26-39 insulin Homo sapiens 94-101 13130391-3 2003 Acetylcholine synthesis depends on the availability of acetyl CoA, provided from glucose breakdown, and insulin, which controls the activity of acetylcholine transferase. Acetylcholine 0-13 insulin Homo sapiens 104-111 12835332-3 2003 Our data demonstrate that insulin (0.6 nmol/L) is able to enhance vasodilation induced by leptin (10(-11) to 10(-6) mol/L; percentage change in maximal vasodilation, 39+/-3% vs 26+/-2%; n=6, P<0.03) but not by acetylcholine. Acetylcholine 213-226 insulin Homo sapiens 26-33 11588141-12 2001 The paper also discusses the mechanisms explaining the glucose dependence of the effects of ACh on insulin release. Acetylcholine 92-95 insulin Homo sapiens 99-106 12791513-3 2003 In eight patients with diabetes mellitus or impaired glucose metabolism, the vasodilatory response to acetylcholine at infusion rates of 7.5, 15, and 30 microg/min was studied in the fasting state and at two levels of hyperglycemia, which were achieved by the infusion of glucose, insulin, and somatostatin. Acetylcholine 102-115 insulin Homo sapiens 281-288 12430784-4 2002 HYPOTHESIS: This study was designed to elucidate the correlation among insulin resistance, remnant lipoproteins, and acetylcholine (ACh)-induced coronary artery response. Acetylcholine 117-130 insulin Homo sapiens 71-78 12430784-4 2002 HYPOTHESIS: This study was designed to elucidate the correlation among insulin resistance, remnant lipoproteins, and acetylcholine (ACh)-induced coronary artery response. Acetylcholine 132-135 insulin Homo sapiens 71-78 11738280-5 2001 RESULTS: When we divided patients into tertiles based on insulin sensitivity, we observed stepwise decreases in the maximal ACh-induced vasodilation and plasma BH(4)/7,8-BH(2) ratio, and increases in coronary LPO production as insulin sensitivity decreased. Acetylcholine 124-127 insulin Homo sapiens 57-64 11738280-5 2001 RESULTS: When we divided patients into tertiles based on insulin sensitivity, we observed stepwise decreases in the maximal ACh-induced vasodilation and plasma BH(4)/7,8-BH(2) ratio, and increases in coronary LPO production as insulin sensitivity decreased. Acetylcholine 124-127 insulin Homo sapiens 227-234 11738280-6 2001 The ACh-induced vasodilation was positively correlated with insulin sensitivity, BH(4)/7,8-BH(2) ratio and DHPR activity. Acetylcholine 4-7 insulin Homo sapiens 60-67 12629115-7 2003 Insulin coinfusion increased acetylcholine-stimulated flow in both groups: 18.0 +/- 3.1 vs. 17.9 +/- 3.1 [ml x (100 ml forearm)(-1) x min(-1)], NS. Acetylcholine 29-42 insulin Homo sapiens 0-7 12469359-15 2002 Agonists that can change the rate-limiting steps for both phases of insulin release include those like glucagon-like peptide 1 (GLP-1) that raise cyclic AMP levels and those like acetylcholine that act via DAG. Acetylcholine 179-192 insulin Homo sapiens 68-75 11956956-5 2002 This abnormality along with a reduction in brain insulin concentration is assumed to induce a cascade-like process of disturbances including cellular glucose, acetylcholine, cholesterol, and ATP associated with abnormalities in membrane pathology and the formation of both amyloidogenic derivatives and hyperphosphorylated tau protein. Acetylcholine 159-172 insulin Homo sapiens 49-56 11872375-4 2002 Indeed, insulin resistant states, which by definition, exhibit diminished insulin-mediated glucose uptake into peripheral tissues also display impaired insulin mediated vasodilation as well as impaired endothelium dependent vasolidation to the muscarinic receptor agonist acetylcholine. Acetylcholine 272-285 insulin Homo sapiens 8-15 11872375-4 2002 Indeed, insulin resistant states, which by definition, exhibit diminished insulin-mediated glucose uptake into peripheral tissues also display impaired insulin mediated vasodilation as well as impaired endothelium dependent vasolidation to the muscarinic receptor agonist acetylcholine. Acetylcholine 272-285 insulin Homo sapiens 74-81 11679442-9 2001 Although neither the ACh response (P = 0.09) nor the SNP response (P = 0.4) had changed significantly, insulin stimulation had a significant effect, as the ACh response increased by 58 +/- 25, 84 +/- 66, 120 +/- 93, and 69 +/- 36% (P = 0.0002). Acetylcholine 156-159 insulin Homo sapiens 103-110 10806013-0 2000 Insulin resistance affects endothelium-dependent acetylcholine-induced coronary artery response. Acetylcholine 49-62 insulin Homo sapiens 0-7 11147782-9 2001 Regression analysis revealed a significant negative correlation between BMI (r = -0.676, P < 0.0001), WHR (r = -0.631, P < 0.0001), fasting insulin (r = -0.695, P < 0.0001), HOMA-IR (r = -0.633, P < 0.0001), and percent peak increase in FBF during ACh infusion. Acetylcholine 260-263 insulin Homo sapiens 146-153 11113614-6 2000 This abnormality along with a reduction in insulin concentration is assumed to induce a cascade-like process of disturbances including decreases in cellular glucose, acetylcholine, cholesterol, and ATP, associated with changes in the metabolism of amino acids and fatty acids. Acetylcholine 166-179 insulin Homo sapiens 43-50 10806013-1 2000 AIMS: This study was designed to investigate the relationship between insulin resistance and the acetylcholine-induced endothelium-dependent coronary artery response in patients without angiographically significant atherosclerotic coronary artery disease and to elucidate the pathophysiological significance of insulin resistance in the early stages of coronary atherosclerosis. Acetylcholine 97-110 insulin Homo sapiens 70-77 10806013-1 2000 AIMS: This study was designed to investigate the relationship between insulin resistance and the acetylcholine-induced endothelium-dependent coronary artery response in patients without angiographically significant atherosclerotic coronary artery disease and to elucidate the pathophysiological significance of insulin resistance in the early stages of coronary atherosclerosis. Acetylcholine 97-110 insulin Homo sapiens 311-318 10669655-4 2000 During insulin therapy, the acetylcholine response increased by 44% to 10.8+/-1.6 mL x dL(-1) x min(-1) (P<0.05). Acetylcholine 28-41 insulin Homo sapiens 7-14 10677386-5 2000 The LDF response to acetylcholine increased during C-peptide infusion and decreased during saline infusion [18.6+/-19.2 and -13.2+/-9.4 arbitrary units respectively; mean+/-S.E.M. Acetylcholine 20-33 insulin Homo sapiens 51-60 9836233-0 1998 Intraportal acetylcholine reverses insulin resistance caused by chronic bile duct ligation. Acetylcholine 12-25 insulin Homo sapiens 35-42 10690315-10 1999 The insulin effect shown was totally reversed by acetylcholine (3 microM) which is known to inhibit adenylyl cyclase activity/cAMP-production via Gi-proteins. Acetylcholine 49-62 insulin Homo sapiens 4-11 10543718-8 1999 Liver disease is often associated with insulin resistance; the bile duct ligation model of liver disease results in parasympathetic neuropathy and insulin resistance that is reversed by intraportal acetylcholine. Acetylcholine 198-211 insulin Homo sapiens 147-154 10027812-8 1999 Capillary recruitment and acetylcholine-mediated vasodilatation were strongly and positively related to insulin sensitivity (r=0.84, P<0.001; r=0.78, P<0.001, respectively), and capillary recruitment was inversely related to 24-hour SBP (r=-0.53, P<0.05). Acetylcholine 26-39 insulin Homo sapiens 104-111 10600665-12 2000 The vasodilator response to acetylcholine was reduced in DM subjects (P<0.05; analysis of variance), and the slope of this dose-flow relationship was inversely related to insulin levels (r(2)=0.2; P<0.05). Acetylcholine 28-41 insulin Homo sapiens 174-181 10600665-14 2000 Diminished vasodilator responses to acetylcholine may also, in part, be a consequence of insulin-augmented resting muscle blood flow. Acetylcholine 36-49 insulin Homo sapiens 89-96 9821657-3 1998 We found that vasodilation in response to acetylcholine, but not to adenosine diphosphate (ADP), histamine or the calcium ionophore A23187, was modestly enhanced after 20-min pretreatment with human insulin (100 nM) whereas endothelium-independent responses to the NO donor sodium nitroprusside were not significantly affected. Acetylcholine 42-55 insulin Homo sapiens 199-206 9440253-5 1997 Acetylcholine at 8 microM augmented insulin release at both levels of glucose, and ouabain potentiated this effect synergistically at high, but not low glucose. Acetylcholine 0-13 insulin Homo sapiens 36-43 9426377-18 1997 CONCLUSIONS: Our present data indicate that in man, as in animals, acetylcholine has a stimulatory influence on insulin secretion. Acetylcholine 67-80 insulin Homo sapiens 112-119 9075065-12 1997 Nevertheless, these findings confirm that acetylcholine positively influences insulin secretion in humans, likely via indirect mechanisms. Acetylcholine 42-55 insulin Homo sapiens 78-85 9264492-7 1997 During the clamp, insulin sensitive patients tended to have greater increments in forearm blood flow when compared to their insulin resistant counterparts (+53+/-21 versus +9+/-7%, P=.06); in the whole group, clamp-induced vasodilatation was weakly related to insulin-mediated glucose uptake (r=.44, P<.02) as well as to the slope of the acetylcholine dose-response curve (r=.40, P<.04). Acetylcholine 341-354 insulin Homo sapiens 18-25 8626958-9 1996 Among patients with vasospastic angina, those with acetylcholine-induced multivessel coronary vasospasm showed a significantly higher sum of insulin concentrations than those with single-vessel spasm (p < 0.01). Acetylcholine 51-64 insulin Homo sapiens 141-148 8751600-6 1996 RESULTS: Infusion of 25 nmol/L and 2.5 mumol/L acetylcholine resulted in a significant stimulation of insulin secretion before NMMA infusion (p < 0.05) and after NMMA infusion for acetylcholine at 25 nmol/L (p < 0.05). Acetylcholine 47-60 insulin Homo sapiens 102-109 8751600-7 1996 There was a significant decrease in acetylcholine-induced insulin secretion after NMMA infusion for acetylcholine at 25 nmol/L and 2.5 mumol/L compared with before NMMA infusion (p < 0.05). Acetylcholine 36-49 insulin Homo sapiens 58-65 8751600-7 1996 There was a significant decrease in acetylcholine-induced insulin secretion after NMMA infusion for acetylcholine at 25 nmol/L and 2.5 mumol/L compared with before NMMA infusion (p < 0.05). Acetylcholine 100-113 insulin Homo sapiens 58-65 8536617-4 1996 Arginine vasopressin (AVP), bombesin, and acetylcholine potentiate glucose-induced insulin secretion and are known to raise cytosolic calcium levels through binding to cell surface receptors that activate phospholipase C. The effect of AVP on CRE-directed transcription was examined in the beta-cell line HIT. Acetylcholine 42-55 insulin Homo sapiens 83-90 1383242-4 1992 Acetyl choline and vasopressin (VP) both potentiate the acute effects of glucose on insulin secretion by generating inositol 1,4,5-trisphosphate to release intracellular Ca2+; VP also potentiates sustained insulin secretion by effects on depolarization. Acetylcholine 0-14 insulin Homo sapiens 84-91 7829788-0 1995 Enhanced insulin response relates to acetylcholine-induced vasoconstriction in vasospastic angina. Acetylcholine 37-50 insulin Homo sapiens 9-16 7829788-1 1995 OBJECTIVES: This study investigated whether insulin response to an oral glucose load correlates to acetylcholine-induced coronary vasoconstriction in subjects with vasospastic angina. Acetylcholine 99-112 insulin Homo sapiens 44-51 7829788-9 1995 CONCLUSIONS: Results show that acetylcholine-induced coronary vasoconstriction in subjects with vasospastic angina correlates with hyperinsulinemia and enhanced insulin response, suggesting insulin resistance syndrome as a feature of vasospastic angina. Acetylcholine 31-44 insulin Homo sapiens 136-143 7586259-0 1995 Effect of insulin on acetylcholine-induced vasodilation in normotensive subjects and patients with essential hypertension. Acetylcholine 21-34 insulin Homo sapiens 10-17 7586259-4 1995 In both normotensive and hypertensive subjects, insulin significantly potentiated acetylcholine-induced vasodilation, whereas it did not alter the vasodilatory response to sodium nitroprusside. Acetylcholine 82-95 insulin Homo sapiens 48-55 7586259-5 1995 NG-monomethyl-L-arginine, an inhibitor of endothelial nitric oxide synthesis, blunted insulin-induced facilitation of acetylcholine vasodilation in normotensive but not in hypertensive subjects. Acetylcholine 118-131 insulin Homo sapiens 86-93 7586259-7 1995 CONCLUSIONS: In healthy humans and essential hypertensive patients alike, local physiological hyperinsulinemia per se does not increase forearm blood flow but potentiates the vasodilation induced by acetylcholine regardless of metabolic insulin resistance. Acetylcholine 199-212 insulin Homo sapiens 99-106 7635265-3 1995 Under these experimental conditions, metabolic (glucose, ketoisocaproic acid, and arginine) and nonmetabolic (K+ and tolbutamide) agents as well as glucagon and acetylcholine significantly stimulated the release of immunoreactive insulin. Acetylcholine 161-174 insulin Homo sapiens 230-237 1383242-4 1992 Acetyl choline and vasopressin (VP) both potentiate the acute effects of glucose on insulin secretion by generating inositol 1,4,5-trisphosphate to release intracellular Ca2+; VP also potentiates sustained insulin secretion by effects on depolarization. Acetylcholine 0-14 insulin Homo sapiens 206-213 1375990-1 1992 Adrenaline, permeable cyclic adenosine monophosphate (cAMP) derivatives and insulin are known to elicit an increase in quantal size at the frog neuromuscular junction, primarily by increasing the amount of acetylcholine (ACh) per quantum. Acetylcholine 206-219 insulin Homo sapiens 76-83 1375990-1 1992 Adrenaline, permeable cyclic adenosine monophosphate (cAMP) derivatives and insulin are known to elicit an increase in quantal size at the frog neuromuscular junction, primarily by increasing the amount of acetylcholine (ACh) per quantum. Acetylcholine 221-224 insulin Homo sapiens 76-83 35447544-6 2022 In addition, histamine H3R antagonists stimulate insulin release, through inducing the release of acetylcholine and cause significant reduction in total body weight and triglycerides in obese subjects by causing a feeling of satiety in the hypothalamus. Acetylcholine 98-111 insulin Homo sapiens 49-56 1816091-0 1991 Effect of intracerebroventricularly administered insulin on brain monoamines and acetylcholine in euglycaemic and alloxan-induced hyperglycaemic rats. Acetylcholine 81-94 insulin Homo sapiens 49-56 1816091-2 1991 Since a number of central neurotransmitters are also known to influence glucose levels and it is likely that CNS insulin receptors act through neurotransmitter mediation, the present study was conducted to investigate the effect of intracerebroventricularly (icv) administered insulin on rat brain dopamine (DA), noradrenaline (NA), serotonin and acetylcholine (ACh) activity in normal and alloxan-induced hyperglycaemic animals. Acetylcholine 347-360 insulin Homo sapiens 113-120 1816091-2 1991 Since a number of central neurotransmitters are also known to influence glucose levels and it is likely that CNS insulin receptors act through neurotransmitter mediation, the present study was conducted to investigate the effect of intracerebroventricularly (icv) administered insulin on rat brain dopamine (DA), noradrenaline (NA), serotonin and acetylcholine (ACh) activity in normal and alloxan-induced hyperglycaemic animals. Acetylcholine 362-365 insulin Homo sapiens 113-120 1816091-9 1991 Insulin induced marked increase in rat brain ACh levels, which was accentuated in hyperglycaemic animals. Acetylcholine 45-48 insulin Homo sapiens 0-7 1816091-10 1991 The present study reports for the first time the likely interaction between CNS insulin receptors and brain monoamines, and ACh, in euglycaemic and hyperglycaemic states. Acetylcholine 124-127 insulin Homo sapiens 80-87 2096884-6 1990 Since the single chain insulin precursor can be produced by gene technology (yeast), use of immobilized trypsin or Ach and the two-step reaction using the single chain insulin precursor as the starting material ensures the continuous production of human insulin making it a feasible method for industrial manufacture. Acetylcholine 115-118 insulin Homo sapiens 23-30