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Chemical Compound Review

Mecholyl     2-acetyloxypropyl-trimethyl- azanium chloride

Synonyms: Provokit, Amechol, Provocholine, Prestwick_981, AG-G-29658, ...
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Disease relevance of methacholine

  • Euglycemic hyperinsulinemia augmented the LBF response to MCh by - 50% in C (P < 0.05 vs saline) but not in OB and NIDDM [1].
  • In the present investigation, cholinergic stimulation was produced by administering the selective muscarinic agent methacholine (MCh) and ventricular vulnerability was assessed by measuring the repetitive extrasystole (RE) threshold [2].
  • Mild airway obstruction and increased airway responsiveness to inhaled MCH but not to MBS suggest that structural changes in distal airways are involved and not autonomic nerve dysfunction [3].
  • Five of the seven patients with FAP showed bronchial hyperreactivity to MCh, and PD20 to MCh was significantly lower than that of the normal subjects (p < 0.01) [4].
  • In mice, respiratory syncytial virus (RSV) infection can enhance the consequences of allergic airway sensitization, resulting in lung eosinophilia and the development of airway hyperresponsiveness (AHR) to inhaled methacholine (MCh) [5].

High impact information on methacholine

  • During the 2-h SRIF infusion, insulin levels fell, and FFA levels rose from 474+/-22 to 1,042+/-116 micromol (P < 0.01); Mch-induced vasodilation was reduced by approximately 20% (P < 0.02, saline vs. SRIF, ANOVA) [6].
  • Mch-induced vasodilation relative to baseline was reduced by approximately 20% in response to the raised FFA levels in both groups (P < 0.05, saline vs. FFA, ANOVA) [6].
  • MCh induced increments in LBF were approximately 40% and 55% lower in OB and NIDDM, respectively, as compared with C (P < 0.05) [1].
  • Regression analysis revealed a significant inverse correlation between the maximal LBF change in response to MCh and body fat content [1].
  • To investigate the cellular sources and the secretory control of these nasal proteins in vivo, 34 adult subjects underwent nasal provocation tests with methacholine (MC), histamine (H), and gustatory stimuli [7].

Chemical compound and disease context of methacholine


Biological context of methacholine

  • Our study showed significant linkage between airway responsiveness to MTCH and D2S1780 on chromosome 2 (P<.00002) and provided suggestive evidence (P<.002) for six additional possible QTLs: D10S1435 and D22S685, for FEV1; D16S412, for FVC; D19S433, for airway responsiveness to MTCH; D1S518, for TIgE; and D4S1647, for skin reactivity to cockroach [12].
  • Maximal isometric contraction to MCh increased from 1911 +/- 245 (Generation 2) to 6693 +/- 850 g/gM (Generation 5) (P less than 0.005) [13].
  • Furthermore, we observed that after constriction had already been induced by MCh, following a DI, bronchodilation occurred in the healthy subjects but further bronchoconstriction occurred in the subjects with asthma [14].
  • Airway function was monitored by changes in lung resistance (RL) and dynamic compliance (Cdyn) to methacholine (MCh) inhalation after anti-VLA-4 [15].
  • In contrast, generation of isometric tension in trachealis, morphometric measurements of tracheal ASM, tracheal myosin content, and dose-response curves for MCh of explanted intraparenchymal bronchi failed to correspond to the in vivo phenotype of airway reactivity [16].

Anatomical context of methacholine

  • Compared with MCh only piglets, the thickness of the outer airway wall (between the outer border of the smooth muscle and the surrounding lung parenchyma) was increased (p < 0.05) in engorged only and engorged plus MCh piglets [17].
  • Airway responsiveness to inhaled MCh was assessed and numbers of lung eosinophils were monitored [5].
  • The influence of pulmonary vascular congestion on the response of the airways and lung tissue to low doses of inhaled methacholine (MCh) was studied by inflating a balloon catheter in the left atrium of the heart in six piglets, with an additional five piglets serving as control animals [17].
  • Perfusion with lipopolysaccharide (LPS) had no effect on pulmonary resistance or pulmonary artery pressure, but induced airway hyperreactivity (AHR) to methacholine (MCh) and pulmonary vascular hyperreactivity (VHR) to platelet-activating factor (PAF) [18].
  • 5. Simultaneous measurement of cytosolic (fluo-3 AM) and mitochondrial (rhod-2 AM) Ca2+ responses revealed that Ca2+ elevations in the cytosol evoked by either MCh or kainate were translated into long-lasting Ca2+ elevations in subpopulations of mitochondria [19].

Associations of methacholine with other chemical compounds


Gene context of methacholine

  • The M2-/- mice showed significantly enhanced in vivo bronchoconstrictor responses to vagal stimulation or MCh administration [23].
  • The reduced hypotensive response of M3-/- mice to MCh suggests M3 mAChRs contribute to peripheral vasodilation [23].
  • The EC50 values for MCh-induced ERK activation in both cell types were essentially identical and similar to that for JNK activation in CHO-m3 cells, suggesting little amplification of the response [24].
  • In response to MCh infusion, both the net release of TPA antigen and increment in TPA activity increased markedly and to similar extents in both groups (P < .01 throughout) [25].
  • In addition, GRK3 -/- mice displayed an altered HR recovery from MCh-induced bradycardia [26].

Analytical, diagnostic and therapeutic context of methacholine

  • Low-dose inhaled MCh (0.3 mg/ml) increased Raw and Rti in the control group by 10.8 +/- 10.3% and 42.2 +/- 29.5%, respectively [17].
  • Recipients were challenged with aerosolized OA or bovine serum albumin (BSA) (5% wt/vol) and analyzed for changes in lung resistance (RL), airway responsiveness to inhaled methacholine (MCh), and bronchoalveolar lavage (BAL) cells [27].
  • Dynamic narrowing of intraparenchymal airways after maximal MCh stimulation was assessed by video microscopy [28].
  • First we examined the FEV1 and Raw in seven patients with FAP and in six normal subjects, then we administered aerosols of increasing concentrations of MCh (0.075 to 25 mg/ml) at about 5-min intervals via a nebulizer controlled by a dosimeter [4].
  • We studied leg blood flow (LBF) responses to graded intrafemoral artery infusion of the endothelium-dependent vasodilator methacholine chloride (MCh) and to a 4-h hyperinsulinemic euglycemic clamp (120 mU/m(2) x min) in 10 PCOS, before and after 3 months treatment with Tgz (600 mg/d) [29].


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  13. Distribution of airway contractile responses in major resistance airways of the dog. Shioya, T., Pollack, E.R., Munoz, N.M., Leff, A.R. Am. J. Pathol. (1987) [Pubmed]
  14. High-resolution computed tomographic evaluation of airway distensibility and the effects of lung inflation on airway caliber in healthy subjects and individuals with asthma. Brown, R.H., Scichilone, N., Mudge, B., Diemer, F.B., Permutt, S., Togias, A. Am. J. Respir. Crit. Care Med. (2001) [Pubmed]
  15. Timing of administration of anti-VLA-4 differentiates airway hyperresponsiveness in the central and peripheral airways in mice. Kanehiro, A., Takeda, K., Joetham, A., Tomkinson, A., Ikemura, T., Irvin, C.G., Gelfand, E.W. Am. J. Respir. Crit. Care Med. (2000) [Pubmed]
  16. Bronchial responsiveness among inbred mouse strains. Role of airway smooth-muscle shortening velocity. Duguet, A., Biyah, K., Minshall, E., Gomes, R., Wang, C.G., Taoudi-Benchekroun, M., Bates, J.H., Eidelman, D.H. Am. J. Respir. Crit. Care Med. (2000) [Pubmed]
  17. Pulmonary vascular congestion selectively potentiates airway responsiveness in piglets. Uhlig, T., Wildhaber, J.H., Carroll, N., Turner, D.J., Gray, P.R., Dore, N., James, A.L., Sly, P.D. Am. J. Respir. Crit. Care Med. (2000) [Pubmed]
  18. Mechanisms of endotoxin-induced airway and pulmonary vascular hyperreactivity in mice. Held, H.D., Uhlig, S. Am. J. Respir. Crit. Care Med. (2000) [Pubmed]
  19. Mitochondrial Ca2+ uptake and release influence metabotropic and ionotropic cytosolic Ca2+ responses in rat oligodendrocyte progenitors. Simpson, P.B., Russell, J.T. J. Physiol. (Lond.) (1998) [Pubmed]
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  21. Release of tissue-type plasminogen activator in response to muscarinic receptor stimulation in human forearm. Jern, S., Selin, L., Bergbrant, A., Jern, C. Thromb. Haemost. (1994) [Pubmed]
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  24. Regulation of extracellular-signal regulated kinase and c-Jun N-terminal kinase by G-protein-linked muscarinic acetylcholine receptors. Wylie, P.G., Challiss, R.A., Blank, J.L. Biochem. J. (1999) [Pubmed]
  25. Endothelium-dependent vasodilation and tissue-type plasminogen activator release in borderline hypertension. Jern, S., Wall, U., Bergbrant, A., Selin-Sjögren, L., Jern, C. Arterioscler. Thromb. Vasc. Biol. (1997) [Pubmed]
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  27. Adoptive transfer of allergic airway responses with sensitized lymphocytes in BN rats. Watanabe, A., Rossi, P., Renzi, P.M., Xu, L.J., Guttmann, R.D., Martin, J.G. Am. J. Respir. Crit. Care Med. (1995) [Pubmed]
  28. Greater velocity and magnitude of airway narrowing in immature than in mature rabbit lung explants. Duguet, A., Wang, C.G., Gomes, R., Ghezzo, H., Eidelman, D.H., Tepper, R.S. Am. J. Respir. Crit. Care Med. (2001) [Pubmed]
  29. Troglitazone therapy improves endothelial function to near normal levels in women with polycystic ovary syndrome. Paradisi, G., Steinberg, H.O., Shepard, M.K., Hook, G., Baron, A.D. J. Clin. Endocrinol. Metab. (2003) [Pubmed]
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