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Journal articles on the topic 'Acetylcholine'

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Published: 4 June 2021

Last updated: 14 September 2024

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1

Barman, S. A., E. Senteno, S. Smith, and A. E. Taylor. "Acetylcholine's effect on vascular resistance and compliance in the pulmonary circulation." Journal of Applied Physiology 67, no. 4 (October 1, 1989): 1495–503. http://dx.doi.org/10.1152/jappl.1989.67.4.1495.

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Acetylcholine's effect on the distribution of vascular resistance and compliance in the canine pulmonary circulation was determined under control and elevated vascular tone by the arterial, venous, and double occlusion techniques in isolated blood-perfused dog lungs at both constant flow and constant pressure. Large and small blood vessel resistances and compliances were studied in lungs given concentrations of acetylcholine ranging from 2.0 ng/ml to 200 micrograms/ml. The results of this study indicate that acetylcholine dilates large arteries at low concentrations (less than or equal to 20 ng/ml) and constricts small and large veins at concentrations of at least 2 micrograms/ml. Characterization of acetylcholine's effects at constant pulmonary blood flow indicates that 1) large artery vasodilation may be endothelial-derived relaxing factor-mediated because the dilation is blocked with methylene blue; 2) a vasodilator of the arachidonic acid cascade (blocked by ibuprofen), probably prostacyclin, lessens acetylcholine's pressor effects; 3) when vascular tone was increased, acetylcholine's hemodynamic effects were attenuated; and 4) acetylcholine decreased middle compartment and large vessle compliance under control but not elevated vascular tone. Under constant pressure at control vascular tone acetylcholine increases resistance in all segments except the large artery, and at elevated vascular tone the pressor effects were enhanced, and large artery resistance was increased.

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2

Xu, Zemin, Chuanyao Tong, and James C. Eisenach. "Acetylcholine Stimulates the Release of Nitric Oxide from Rat Spinal Cord." Anesthesiology 85, no. 1 (July 1, 1996): 107–11. http://dx.doi.org/10.1097/00000542-199607000-00015.

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Background Acetylcholine causes synthesis of nitric oxide in vascular endothelium, and presumptive evidence in vivo suggests spinally released acetylcholine causes antinociception and increased sympathetic nervous system activity via a nitric oxide mechanism. The purpose of this study was to determine, using a recently described bioassay system, whether acetylcholine stimulates nitric oxide release from spinal cord tissue in vitro. Methods Rat thoracolumbar spinal cord slices were incubated in a tissue chamber and perfused with Krebs-Henseleit solution. The perfusate was then passed through endotheliumdenuded rat aortic rings and their tension was measured. Vascular rings were preconstricted with phenylephrine, then were exposed to spinal cord perfusate with increasing concentrations (10(-12)-10(-4)M) of acetylcholine alone or with various antagonists. Results Acetylcholine perfusion of spinal tissue caused concentration-dependent relaxations of the aortic rings, an effect blocked by each of the muscarinic antagonists, atropine, pirenzepine, and AFDX-116. Acetylcholine-induced relaxation also was antagonized by an inhibitor of nitric oxide synthase (N-methyl-L-arginine), a nitric oxide scavenger (hemoglobin) and an inhibitor of guanylate cyclase (methylene blue). Conclusions These results demonstrate release of a vasorelaxant from spinal cord tissue by acetylcholine, which results from an action on muscarinic receptors and exhibits a pharmacology consistent with nitric oxide. Although precise anatomic localization of acetylcholine's action is not possible with this system, these results add to evidence that acetylcholine causes nitric oxide synthesis in the spinal cord.

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3

&NA;. "Acetylcholine." Reactions Weekly &NA;, no. 1146-1147 (April 2007): 6. http://dx.doi.org/10.2165/00128415-200711460-00018.

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4

&NA;. "Acetylcholine." Reactions Weekly &NA;, no. 471 (October 1993): 5. http://dx.doi.org/10.2165/00128415-199304710-00021.

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&NA;. "Acetylcholine." Reactions Weekly &NA;, no. 380 (December 1991): 3. http://dx.doi.org/10.2165/00128415-199103800-00006.

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6

&NA;. "Acetylcholine." Reactions Weekly &NA;, no. 952 (May 2003): 6. http://dx.doi.org/10.2165/00128415-200309520-00019.

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7

Brown, David A. "Acetylcholine." British Journal of Pharmacology 147, S1 (January 2006): S120—S126. http://dx.doi.org/10.1038/sj.bjp.0706474.

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8

Doliba, Nicolai M., Wei Qin, Sergei A. Vinogradov, David F. Wilson, and Franz M. Matschinsky. "Palmitic acid acutely inhibits acetylcholine- but not GLP-1-stimulated insulin secretion in mouse pancreatic islets." American Journal of Physiology-Endocrinology and Metabolism 299, no. 3 (September 2010): E475—E485. http://dx.doi.org/10.1152/ajpendo.00072.2010.

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Fatty acids, acetylcholine, and GLP-1 enhance insulin secretion in a glucose-dependent manner. However, the interplay between glucose, fatty acids, and the neuroendocrine regulators of insulin secretion is not well understood. Therefore, we studied the acute effects of PA (alone or in combination with glucose, acetylcholine, or GLP-1) on isolated cultured mouse islets. Two different sets of experiments were designed. In one, a fixed concentration of 0.5 mM of PA bound to 0.15 mM BSA was used; in the other, a PA ramp from 0 to 0.5 mM was applied at a fixed albumin concentration of 0.15 mM so that the molar PA/BSA ratio changed within the physiological range. At a fixed concentration of 0.5 mM, PA markedly inhibited acetylcholine-stimulated insulin release, the rise of intracellular Ca2+, and enhancement of cAMP production but did not influence the effects of GLP-1 on these parameters of islet cell function. 2-ADB, an IP3 receptor inhibitor, reduced the effect of acetylcholine on insulin secretion and reversed the effect of PA on acetylcholine-stimulated insulin release. Islet perfusion for 35–40 min with 0.5 mM PA significantly reduced the calcium storage capacity of ER measured by the thapsigargin-induced Ca2+ release. Oxygen consumption due to low but not high glucose was reduced by PA. When a PA ramp from 0 to 0.5 mM was applied in the presence of 8 mM glucose, PA at concentrations as low as 50 μM significantly augmented glucose-stimulated insulin release and markedly reduced acetylcholine's effects on hormone secretion. We thus demonstrate that PA acutely reduces the total oxygen consumption response to glucose, glucose-dependent acetylcholine stimulation of insulin release, Ca2+, and cAMP metabolism, whereas GLP-1's actions on these parameters remain unaffected or potentiated. We speculate that acute emptying of the ER calcium by PA results in decreased glucose stimulation of respiration and acetylcholine potentiation of insulin secretion.

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9

Seitz, Andreas, Rutger G. T. Feenstra, Regina E. Konst, Valeria Martínez Pereyra, Sascha Beck, Marcel A. M. Beijk, Tim P. van de Hoef, et al. "Acetylcholine Rechallenge." JACC: Cardiovascular Interventions 15, no. 1 (January 2022): 65–75. http://dx.doi.org/10.1016/j.jcin.2021.10.003.

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10

Vogt, Nina. "Detecting acetylcholine." Nature Methods 15, no. 9 (August 31, 2018): 648. http://dx.doi.org/10.1038/s41592-018-0131-y.

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11

Libow, Leslie S. "Acetylcholine Memories." Journal of the American Geriatrics Society 63, no. 7 (July 2015): 1469. http://dx.doi.org/10.1111/jgs.13514.

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12

Björklund, Anders, and Stephen B. Dunnett. "Acetylcholine revisited." Nature 375, no. 6531 (June 1995): 446. http://dx.doi.org/10.1038/375446a0.

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13

Ogura, T. "Acetylcholine and Acetylcholine Receptors in Taste Receptor Cells." Chemical Senses 30, Supplement 1 (January 1, 2005): i41. http://dx.doi.org/10.1093/chemse/bjh103.

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14

Ojeda, Ana M., Natalia G. Kolmakova, and Stanley M. Parsons. "Acetylcholine Binding Site in the Vesicular Acetylcholine Transporter†." Biochemistry 43, no. 35 (September 2004): 11163–74. http://dx.doi.org/10.1021/bi049562b.

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15

Liu, Julia Yuen Hang, Peng Du, and John Anthony Rudd. "Acetylcholine exerts inhibitory and excitatory actions on mouse ileal pacemaker activity: role of muscarinic versus nicotinic receptors." American Journal of Physiology-Gastrointestinal and Liver Physiology 319, no. 1 (July 1, 2020): G97—G107. http://dx.doi.org/10.1152/ajpgi.00003.2020.

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The study discovered an acute action of acetylcholine on pacemaker potentials that is mediated by muscarinic receptors on the mouse ileum. Bethanechol, but not nicotine, mimicked the inhibitory actions of acetylcholine on pacemaker potentials. Atropine, but not hexamethonium, reversed the inhibitory actions of acetylcholine. When introduced after acetylcholine, atropine exhibited excitatory actions that increased the pacemaker frequency. Acetylcholine and bethanechol distorted the propagation activity and pattern, and this was also reversed by atropine. These actions of acetylcholine on pacemaker potentials may contribute to pathophysiology in bowel diseases.

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16

Tsetlin, Victor I. "Acetylcholine and Acetylcholine Receptors: Textbook Knowledge and New Data." Biomolecules 10, no. 6 (June 3, 2020): 852. http://dx.doi.org/10.3390/biom10060852.

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17

Molenaar, P. C., B. S. Oen, R. L. Polak, and A. L. van der Laaken. "Surplus acetylcholine and acetylcholine release in the rat diaphragm." Journal of Physiology 385, no. 1 (April 1, 1987): 147–67. http://dx.doi.org/10.1113/jphysiol.1987.sp016489.

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18

Ma, Yuanyuan, Xianxian Li, Jing Fu, Yue Li, Li Gao, Ling Yang, Ping Zhang, Jiefei Shen, and Hang Wang. "Acetylcholine affects osteocytic MLO-Y4 cells via acetylcholine receptors." Molecular and Cellular Endocrinology 384, no. 1-2 (March 2014): 155–64. http://dx.doi.org/10.1016/j.mce.2014.01.021.

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19

Bhattachayay, Dipankar, Priyabrata Pal, Saikat Banerjee, Shyamal Kanti Sanyal, A. P. F. Turner, and Priyabrata Sarkar. "Electrochemical Acetylcholine Chloride Biosensor Using an Acetylcholine Esterase Biomimic." Analytical Letters 41, no. 8 (June 16, 2008): 1387–97. http://dx.doi.org/10.1080/00032710802119251.

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20

Behling, R. W., T. Yamane, G. Navon, and L. W. Jelinski. "Conformation of acetylcholine bound to the nicotinic acetylcholine receptor." Proceedings of the National Academy of Sciences 85, no. 18 (September 1, 1988): 6721–25. http://dx.doi.org/10.1073/pnas.85.18.6721.

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21

Febriana, Fitri Noor, Vera Khoirunisa, Wun Fui Mark-Lee, and Febdian Rusydi. "Theoretical Study of the Stability of Acetylcholine Based on Molecular Orbital Theory using Density Functional Theory." Indonesian Applied Physics Letters 3, no. 1 (October 31, 2022): 16–19. http://dx.doi.org/10.20473/iapl.v3i1.39777.

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Some molecules in nature have a positive or negative charge. One such molecule is acetylcholine. Acetylcholine is a positively charged molecule that is responsible for Alzheimer's disease. This study evaluated acetylcholine through six simple molecules based on the ionization potential and the HOMO-LUMO gap obtained from the density functional theory calculation. The calculation results showed that the ionization potential and the HOMO-LUMO gap could explain the stability of acetylcholine and the six other molecules. As a result, acetylcholine has the same properties as five other simple molecules. Meanwhile, one other molecule has the opposite properties to acetylcholine.

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22

Collier, Joe, and Patrick Vallance. "Biphasic response to acetylcholine in human veins in vivo: the role of the endothelium." Clinical Science 78, no. 1 (January 1, 1990): 101–4. http://dx.doi.org/10.1042/cs0780101.

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1. The dose-response to acetylcholine has been examined in dorsal hand veins of healthy volunteers before and after removal of the endothelium. 2. Measurements were made in single dorsal hand veins during local infusions of acetylcholine. The vein was irrigated with distilled water to remove the endothelium. Dilator studies were performed in vessels preconstricted by a continuous infusion of noradrenaline. 3. In the endothelium-intact vessel the dose-response to acetylcholine was biphasic; low doses produced venodilatation with higher doses causing venoconstriction. 4. Dilatation to low doses of acetylcholine was abolished by prior irrigation with distilled water, consistent with denudation of the endothelium by this process. Irrigation augmented the constriction seen in response to higher doses of acetylcholine. 5. This is the first demonstration of an endothelium-dependent biphasic dose-response to acetylcholine in man. The results raise questions as to the possible physiological actions of endogenous acetylcholine and as to the use of the acetylcholine dose-response curve as a marker of endothelial function.

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23

Rajendran, Ranjith, Elisa Borghi, Monica Falleni, Federica Perdoni, Delfina Tosi, David F. Lappin, Lindsay O'Donnell, Darren Greetham, Gordon Ramage, and Christopher Nile. "Acetylcholine Protects against Candida albicans Infection by Inhibiting Biofilm Formation and Promoting Hemocyte Function in a Galleria mellonella Infection Model." Eukaryotic Cell 14, no. 8 (June 19, 2015): 834–44. http://dx.doi.org/10.1128/ec.00067-15.

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ABSTRACT Both neuronal acetylcholine and nonneuronal acetylcholine have been demonstrated to modulate inflammatory responses. Studies investigating the role of acetylcholine in the pathogenesis of bacterial infections have revealed contradictory findings with regard to disease outcome. At present, the role of acetylcholine in the pathogenesis of fungal infections is unknown. Therefore, the aim of this study was to determine whether acetylcholine plays a role in fungal biofilm formation and the pathogenesis of Candida albicans infection. The effect of acetylcholine on C. albicans biofilm formation and metabolism in vitro was assessed using a crystal violet assay and phenotypic microarray analysis. Its effect on the outcome of a C. albicans infection, fungal burden, and biofilm formation were investigated in vivo using a Galleria mellonella infection model. In addition, its effect on modulation of host immunity to C. albicans infection was also determined in vivo using hemocyte counts, cytospin analysis, larval histology, lysozyme assays, hemolytic assays, and real-time PCR. Acetylcholine was shown to have the ability to inhibit C. albicans biofilm formation in vitro and in vivo . In addition, acetylcholine protected G. mellonella larvae from C. albicans infection mortality. The in vivo protection occurred through acetylcholine enhancing the function of hemocytes while at the same time inhibiting C. albicans biofilm formation. Furthermore, acetylcholine also inhibited inflammation-induced damage to internal organs. This is the first demonstration of a role for acetylcholine in protection against fungal infections, in addition to being the first report that this molecule can inhibit C. albicans biofilm formation. Therefore, acetylcholine has the capacity to modulate complex host-fungal interactions and plays a role in dictating the pathogenesis of fungal infections.

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24

Sorota, S., and B. F. Hoffman. "Role of G proteins in the acetylcholine-induced potassium current of canine atrial cells." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 5 (November 1, 1989): H1516—H1522. http://dx.doi.org/10.1152/ajpheart.1989.257.5.h1516.

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The acetylcholine-induced opening of potassium channels depends on GTP-binding proteins in the chick, guinea pig, frog, and rat. In contrast, Bubien and Woods (Biochem. Biophys. Res. Commun. 142: 1039-1045, 1987) have recently postulated that the acetylcholine response in cultured canine atrial cells may be independent of GTP-binding proteins. In whole cell patch-clamp experiments using cultured canine atrial cells, we did not detect an effect of GTP (10(-4) M) in the pipette solution on the acetylcholine-induced potassium current. However, 500 microM guanosine 5'-O-(2-thiodiphosphate) (GDP beta S) in the pipette diminished the response to acetylcholine. Pertussis toxin (30 ng/ml for 24 h) blocked the response to acetylcholine. With guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S; 3 microM) in the patch pipette, acetylcholine irreversibly increased membrane conductance. The current-voltage relationship for the persistently activated current was similar to that induced by acetylcholine. We conclude that the acetylcholine-induced potassium current in canine atrial cells behaves like that seen in other species and depends on GTP-binding proteins.

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25

Chowienczyk, P. J., J. R. Cockcroft, and J. M. Ritter. "Blood Flow Responses to Intra-Arterial Acetylcholine in Man: Effects of Basal Flow and Conduit Vessel Length." Clinical Science 87, no. 1 (July 1, 1994): 45–51. http://dx.doi.org/10.1042/cs0870045.

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1. Acetylcholine relaxes human resistance vessels and releases nitric oxide and other factors from the endothelium. Comparison of responses to acetylcholine with those to an endothelium-independent vasodilator (such as nitroprusside) forms the basis of the so-called acetylcholine test of endothelial function. However, when this test is applied in vivo by intraarterial infusion, the metabolic instability of acetylcholine may result in differential responses to these drugs arising from anatomical rather than functional differences. 2. Vasodilator responses to brachial Artery infusions of acetylcholine (41 and 83 nmol/min) and sodium nitroprusside (11 and 38 nmol/min) were measured in 30 healthy human subjects using venous occlusion plethysmography. 3. Responses to acetylcholine showed a greater dependence on resting blood flow (P < 0.05) and on forearm length (P < 0.05) than those to sodium nitroprusside (results predicted by a simple blood flow model). 4. Correction for forearm length abolished an apparent difference of 59% between responses to acetylcholine in men and women. Conduit vessel geometry and resting blood flow influence the acetylcholine test of endothelial function.

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26

Safaei, Mohadeseh. "A Sensitive Voltammetric Sensor Based on Au Nanoparticle Decorated Graphene Nanosheets Modified Glassy Carbon Electrode for Determination of Acetylcholine in Presence of Dopamine." Nanoarchitectonics 1, no. 1 (January 4, 2020): 43–52. http://dx.doi.org/10.37256/nat.112020182.43-52.

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In this study the electro oxidation of acetylcholine (ACh) in pH 7.0 phosphate buffer solution (PBS) was investigated using cyclic voltammetry (CV) and differential pulse voltammetry (DPV) with the modified glassy carbon electrode (GCE) by Au nanoparticle decorated graphene nanosheets (Au NPs/GNs). DPV is a rapid and sensitive electro analytical technique for determination of acetylcholine in presence of dopamine (DA). Using DPV technique, the current was linear within a concentration range of 0.1-700.0 µM of acetylcholine. The detection limit of the method for acetylcholine is 0.04 µM (S/N=3). Diffusion coefficient, D, and charge transfer coefficients, α, have been determined for oxidizing acetylcholine at the modified surface. The applicability of the proposed method was shown by the successful analysis of acetylcholine in real sample.

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27

Wetzel, G. T., and J. H. Brown. "Presynaptic modulation of acetylcholine release from cardiac parasympathetic neurons." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 1 (January 1, 1985): H33—H39. http://dx.doi.org/10.1152/ajpheart.1985.248.1.h33.

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Acetylcholine can be released from parasympathetic nerve endings in rat atria by 57 mM K+ depolarization or by electrical field stimulation. We have studied the presynaptic modulation of [3H]acetylcholine release from superfused rat atria prelabeled with [3H]choline. Exogenous acetylcholine and the specific muscarinic agonist oxotremorine inhibit the stimulation-induced overflow of [3H]acetylcholine into the superfusion medium. The half-maximal inhibitory concentration (IC50) of oxotremorine is 0.3 microM. The cholinesterase inhibitor neostigmine also decreases K+-stimulated [3H]acetylcholine overflow, whereas the muscarinic antagonist atropine enhances the overflow of [3H]acetylcholine. These data suggest that acetylcholine release in atria is modulated through negative feedback by the endogenous transmitter. The sympathetic adrenergic neurotransmitter norepinephrine and the neurohormone epinephrine also inhibit the overflow of [3H]acetylcholine by approximately 60%. The IC50 values for the inhibitory effects of these catecholamines are 6.3 and 2.2 microM, respectively. The inhibitory effect of norepinephrine is blocked by the alpha-adrenergic receptor antagonist yohimbine but not by the beta-adrenergic receptor antagonist propranolol. We suggest that presynaptic muscarinic and alpha-adrenergic receptors participate in the physiological and pharmacological control of cardiac parasympathetic activity.

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Phillips, Joy A., Alex Horkowitz, and Ralph Feuer. "Acetylcholine and Cholinergic Lymphocytes in the Immune Response to Influenza." Journal of Immunology 202, no. 1_Supplement (May 1, 2019): 66.20. http://dx.doi.org/10.4049/jimmunol.202.supp.66.20.

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Abstract Acetylcholine acts to control inflammation in part via binding to α7 nicotinic acetylcholine, receptors on inflammatory macrophages, inhibiting NF-κB nuclear translocation and down-regulating ongoing inflammatory cytokine synthesis. This pathway is presumed to function in the lungs, but the source of local acetylcholine in response to pulmonary inflammation is as yet unknown. We have found evidence that the airway acetylcholine concentration increases over the course of influenza infection, peaking 10 days after infection before rapidly decreasing. The kinetics of acetylcholine increase and loss is mirrored by the appearance and disappearance of cholinergic CD4 T cells in the lungs and airways during influenza illness and resolution. These CD4 T cells bind to influenza-specific tetramers, indicating antigen specificity. This is the first evidence for cholinergic lymphocyte participation in the response to respiratory viral infection. The role for acetylcholine during infleunza recovery is as yet unknown. Decreasing the airway acetylcholine concentration at the later stages of influenza infection leads to extended inflammation marked by increased expression of Allograft-inhibitory factor 1 (Aif-1, IBA1). Together, the results indicate that acetylcholine produced by cholinergic lymphocytes act to regulate pulmonary inflammation during viral infection.

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Horibe, Mayumi, Koji Ogawa, Ju-Tae Sohn, and Paul A. Murray. "Propofol Attenuates Acetylcholine-induced Pulmonary Vasorelaxation." Anesthesiology 93, no. 2 (August 1, 2000): 447–55. http://dx.doi.org/10.1097/00000542-200008000-00024.

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Background The mechanism by which propofol selectively attenuates the pulmonary vasodilator response to acetylcholine is unknown. The goals of this study were to identify the contributions of endogenous endothelial mediators (nitric oxide [NO], prostacyclin, and endothelium-derived hyperpolarizing factors [EDHFs]) to acetylcholine-induced pulmonary vasorelaxation, and to delineate the extent to which propofol attenuates responses to these endothelium-derived relaxing factors. Methods Canine pulmonary arterial rings were suspended for isometric tension recording. The effects of propofol on the vasorelaxation responses to acetylcholine, bradykinin, and the guanylyl cyclase activator, SIN-1, were assessed in phenylephrine-precontracted rings. The contributions of NO, prostacyclin, and EDHFs to acetylcholine-induced vasorelaxation were assessed in control and propofol-treated rings by pretreating the rings with a NO synthase inhibitor (l-NAME), a cyclooxygenase inhibitor (indomethacin), and a cytochrome P450 inhibitor (clotrimazole or SKF 525A) alone and in combination. Results Propofol caused a dose-dependent rightward shift in the acetylcholine dose-response relation, whereas it had no effect on the pulmonary vasorelaxant responses to bradykinin or SIN-1. Cyclooxygenase inhibition only attenuated acetylcholine-induced relaxation at high concentrations of the agonist. NO synthase inhibition and cytochrome P450 inhibition each attenuated the response to acetylcholine, and combined inhibition abolished the response. Propofol further attenuated acetylcholine-induced relaxation after NO synthase inhibition and after cytochrome P450 inhibition. Conclusion These results suggest that acetylcholine-induced pulmonary vasorelaxation is mediated by two components: NO and a cytochrome P450 metabolite likely to be an EDHF. Propofol selectively attenuates acetylcholine-induced relaxation by inhibiting both of these endothelium-derived mediators.

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30

Qin, Xinyue, Herman Kwansa, Enrico Bucci, Sylvain Doré, Darren Boehning, David Shugar, and Raymond C. Koehler. "Role of heme oxygenase-2 in pial arteriolar response to acetylcholine in mice with and without transfusion of cell-free hemoglobin polymers." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 2 (August 2008): R498—R504. http://dx.doi.org/10.1152/ajpregu.00188.2008.

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Carbon monoxide derived from heme oxygenase (HO) may participate in cerebrovascular regulation under specific circumstances. Previous work has shown that HO contributes to feline pial arteriolar dilation to acetylcholine after transfusion of a cell-free polymeric hemoglobin oxygen carrier. The role of constitutive HO2 in the pial arteriolar dilatory response to acetylcholine was determined by using 1) HO2-null mice (HO2−/−), 2) the HO inhibitor tin protoporphyrin IX (SnPPIX), and 3) 4,5,6,7-tetrabromobenzotriazole (TBB), an inhibitor of casein kinase-2 (CK2)-dependent phosphorylation of HO2. In anesthetized mice, superfusion of a cranial window with SnPPIX decreased arteriolar dilation produced by 10 μM acetylcholine by 51%. After partial polymeric hemoglobin exchange transfusion, the acetylcholine response was normal but was reduced 72% by SnPPIX and 95% by TBB. In HO2−/− mice, the acetylcholine response was modestly reduced by 14% compared with control mice and was unaffected by SnPPIX. After hemoglobin transfusion in HO2−/− mice, acetylcholine responses were also unaffected by SnPPIX and TBB. In contrast, nitric oxide synthase inhibition completely blocked the acetylcholine responses in hemoglobin-transfused HO2−/− mice. We conclude 1) that HO2 activity partially contributes to acetylcholine-induced pial arteriolar dilation in mice, 2) that this contribution is augmented in the presence of a plasma-based hemoglobin polymer and appears to depend on a CK2 kinase mechanism, 3) that nitric oxide synthase activity rather than HO1 activity contributes to the acetylcholine reactivity in HO2−/− mice, and 4) that plasma-based polymeric hemoglobin does not scavenge all of the nitric oxide generated by cerebrovascular acetylcholine stimulation.

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31

Ding, Xueqin, and Paul A. Murray. "Acetylcholine Activates Protein Kinase C-α in Pulmonary Venous Smooth Muscle." Anesthesiology 106, no. 3 (March 1, 2007): 507–14. http://dx.doi.org/10.1097/00000542-200703000-00015.

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Background The authors investigated whether acetylcholine-induced contraction in pulmonary venous smooth muscle (PVSM) is associated with the activation of specific protein kinase C (PKC) isoforms. Methods Isolated canine pulmonary venous rings without endothelium were suspended in modified Krebs-Ringer's buffer for measurement of isometric tension. The effects of nonspecific PKC inhibition (bisindolylmaleimide I; 3 x 10 m) and conventional PKC isoform inhibition (Gö7936 10 m) on the acetylcholine dose-response relation were assessed. The expression of conventional PKC isoforms (alpha, beta, gamma), novel PKC isoforms (delta, epsilon, theta), and atypical PKC isoforms (zeta, iota, mu) was measured in PVSM cells by Western blot analysis. The immunofluorescence technique and confocal microscopy were used to localize the cellular distribution of PKC isoforms before and after the addition of acetylcholine. Results Acetylcholine caused dose-dependent contraction in E-pulmonary veins. Pretreatment with bisindolylmaleimide I or Gö7936 attenuated acetylcholine contraction. PKC-alpha, -iota, -mu, and -zeta were expressed, whereas PKC-beta, -gamma, -delta, -epsilon;, and -theta were not expressed in PVSM cells. Immunofluorescence staining for PKC isoforms showed that in unstimulated cells, PKC-alpha and PKC-mu were detected only in the cytoplasm. PKC-iota and PKC-zeta also exhibited a cytoplasmic immunofluorescence pattern, which was especially abundant in the perinuclear zone. Activation with acetylcholine induced translocation of PKC-alpha from cytoplasm to membrane, whereas acetylcholine had no effect on the other PKC isoforms. Translocation of PKC-alpha in response to acetylcholine was blocked by the muscarinic receptor antagonist, atropine. Conclusion Acetylcholine contraction is attenuated by PKC inhibition in PVSM. Acetylcholine induces translocation of PKC-alpha from cytoplasm to membrane in PVSM. These results suggest that PKC-dependent acetylcholine contraction in PVSM may involve activation and translocation of PKC-alpha.

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32

Ford, Thomas J., and Philopatir Mikhail. "Acetylcholine (Re)challenge." JACC: Cardiovascular Interventions 15, no. 1 (January 2022): 76–79. http://dx.doi.org/10.1016/j.jcin.2021.11.022.

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33

King, RG, NM Gude, BR Krishna, S. Chen, SP Brennecke, AL Boura, and TJ Rook. "Human placental acetylcholine." Reproduction, Fertility and Development 3, no. 4 (1991): 405. http://dx.doi.org/10.1071/rd9910405.

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The human placenta contains both acetylcholine (ACh) and choline acetyltransferase, and in vitro bilaterally perfused placental lobules release ACh. The function of this placental cholinergic system has not yet been clearly defined, although changes occur in it during parturition and it may be linked to placental prostaglandin generation at this time. It has also been suggested that ACh may regulate placental amino-acid transport and/or blood flow. It has been found that ACh release from fetal vessels of bilaterally perfused placental lobules is reduced during preeclampsia but is not necessarily correlated with any change in perfusion pressure or materno-fetal transfer of the nonmetabolizable amino acid alpha-aminoisobutyric acid. However, a correlation has been found between releases from human placental explants of ACh (when inhibited by (2-benzoylethyl)trimethylammonium or vesamicol) and of prostaglandins E2 and F2 alpha. Thus, although the evidence for a role of ACh in the control of placental amino-acid transfer or vascular tone is not conclusive, inhibition of the human placental cholinergic system has been shown to be associated with reduced output of prostaglandins from this tissue.

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34

&NA;. "Acetylcholine receptor antagonists." Reactions Weekly &NA;, no. 968 (September 2003): 6. http://dx.doi.org/10.2165/00128415-200309680-00019.

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Wonnacott, Sue, Isabel Bermudez, Neil S. Millar, and Socrates J. Tzartos. "Nicotinic acetylcholine receptors." British Journal of Pharmacology 175, no. 11 (June 2018): 1785–88. http://dx.doi.org/10.1111/bph.14209.

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36

Scott, J. T., David Levy, Ralph Abraham, David Price, B. J. Liddle, and R. E. J. Ryder. "ACETYLCHOLINE SWEATSPOT TEST." Lancet 332, no. 8606 (August 1988): 339–40. http://dx.doi.org/10.1016/s0140-6736(88)92399-9.

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37

Kennedy, WilliamR, and Xavier Navarro. "ACETYLCHOLINE SWEATSPOT TEST." Lancet 332, no. 8614 (October 1988): 789–90. http://dx.doi.org/10.1016/s0140-6736(88)92432-4.

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Klinkenberg, Inge, Anke Sambeth, and Arjan Blokland. "Acetylcholine and attention." Behavioural Brain Research 221, no. 2 (August 2011): 430–42. http://dx.doi.org/10.1016/j.bbr.2010.11.033.

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39

Hasselmo, Michael E., and James M. Bower. "Acetylcholine and memory." Trends in Neurosciences 16, no. 6 (June 1993): 218–22. http://dx.doi.org/10.1016/0166-2236(93)90159-j.

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40

Corringer, Pierre-Jean, and Jean-Pierre Changeux. "Nicotinic acetylcholine receptors." Scholarpedia 3, no. 1 (2008): 3468. http://dx.doi.org/10.4249/scholarpedia.3468.

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41

Liu, Yu, Benjamin J. Scherlag, Youqi Fan, Wenfang Xia, He Huang, and Sunny S. Po. "Acetylcholine–Atropine Interactions." Journal of Cardiovascular Pharmacology 69, no. 6 (June 2017): 369–73. http://dx.doi.org/10.1097/fjc.0000000000000484.

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42

Ishii, Masaru, and Yoshihisa Kurachi. "Muscarinic Acetylcholine Receptors." Current Pharmaceutical Design 12, no. 28 (October 1, 2006): 3573–81. http://dx.doi.org/10.2174/138161206778522056.

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Lee, C. "CONFORMATIONS OF ACETYLCHOLINE." Anesthesiology 89, Supplement (September 1998): 1001A. http://dx.doi.org/10.1097/00000542-199809170-00030.

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Tune, Larry E., and Susan Egeli. "Acetylcholine and Delirium." Dementia and Geriatric Cognitive Disorders 10, no. 5 (1999): 342–44. http://dx.doi.org/10.1159/000017167.

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45

Varoqui, Hélène, and Jeffrey D. Erickson. "Active Transport of Acetylcholine by the Human Vesicular Acetylcholine Transporter." Journal of Biological Chemistry 271, no. 44 (November 1, 1996): 27229–32. http://dx.doi.org/10.1074/jbc.271.44.27229.

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46

Neumann, Eberhard, Elvira Boldt, Barbara Rauer, Hendrik Wolf, and Hai Won Chang. "Scanning curves and kinetics of the acetylcholine/acetylcholine receptor hysteresis." Bioelectrochemistry and Bioenergetics 20, no. 1-3 (December 1988): 45–56. http://dx.doi.org/10.1016/s0302-4598(98)80004-4.

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Siara, J., J. P. Ruppersberg, and R. Rüdel. "Human acetylcholine receptors desensitize much faster than rat acetylcholine receptors." Neuroscience Letters 103, no. 3 (September 1989): 298–302. http://dx.doi.org/10.1016/0304-3940(89)90116-x.

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Wessler, Ignaz, Rosmarie Michel-Schmidt, and Charles James Kirkpatrick. "pH-dependent hydrolysis of acetylcholine: Consequences for non-neuronal acetylcholine." International Immunopharmacology 29, no. 1 (November 2015): 27–30. http://dx.doi.org/10.1016/j.intimp.2015.04.039.

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Deflorio, Cristina, Myriam Catalano, Sergio Fucile, Cristina Limatola, and Francesca Grassi. "Fluoxetine prevents acetylcholine-induced excitotoxicity blocking human endplate acetylcholine receptor." Muscle & Nerve 49, no. 1 (July 15, 2013): 90–97. http://dx.doi.org/10.1002/mus.23870.

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50

Neumann, Eberhard, Elvira Boldt, Barbara Rauer, Hendrik Wolf, and Hai Won Chang. "Scanning curves and kinetics of the acetylcholine / acetylcholine receptor hysteresis." Journal of Electroanalytical Chemistry and Interfacial Electrochemistry 254, no. 1-3 (December 1988): 45–56. http://dx.doi.org/10.1016/0022-0728(80)80333-0.

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