ISSN:
1440-1681
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
1. The histamine H1 and/or H2-receptor agonists showed weak acetylcholinesterase inhibitory activity. Their dissociation constants (Kis and/or Kii) were 2-methyl histamine (Kis= 1751 μmol/1, s.e. = 163) 〈 4-methyl histamine (Kis= 3551 μmol/1, s.e. = 414) 〈 dimaprit (Kis= 2931 μmol/1, s.e. = 605; Kii= 3668 μmol/1, s.e. = 901) 〈 histamine (Kis= 6480 μmol/1, s.e. = 1360).2. Both histamine H1 and H2-receptor antagonists showed stronger acetylcholin-esterase inhibitory activity. Their dissociation constants were ranitidine (Kii= 1.56 μmol/1, s.e. = 0.14) ≪ oxmetidine (Kis= 14.7 μmol/1, s.e. = 1) 〈 mepyramine (Kis= 178 μmol/1, s.e. = 23; Kii= 440 μmol/1, s.e. = 98) 〈 cimetidine (Kis= 199 μmol/1, s.e. = 12; Kii= 827 μmol/1, s.e. = 126).3. Using the ROSFIT programs for fitting data to common enzyme kinetic models, the inhibition caused by histamine, 4-methyl histamine, 2-methyl histamine, oxmetidine and neostigmine was of the competitive type. Mepyramine, cimetidine and dimaprit appeared to exhibit the modern non-competitive type of inhibition with their primary action on the enzyme rather than on the enzyme-substrate complex. Ranitidine seemed to act on the enzyme-substrate complex rather than the enzyme, conforming to the uncompetitive inhibition model.4. The clinical implications of acetylcholinesterase inhibition by cimetidine and ranitidine are discussed.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1440-1681.1985.tb00915.x
Permalink