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THE EFFECTS OF ANTICHOLINESTERASES ON SYNAPTIC TRANSMISSION THROUGH NICOTINIC AND MUSCARINIC RECEPTORS IN RAT SYMPATHETIC GANGLIA in vivo
Author(s) -
DREW G.M.,
LEACH G.D.H.
Publication year - 1974
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1974.tb09686.x
Subject(s) - muscarinic acetylcholine receptor , neuroscience , nicotinic agonist , neurotransmission , in vivo , chemistry , acetylcholine , receptor , biology , endocrinology , biochemistry , microbiology and biotechnology
1 Stimulation of the entire spinal sympathetic outflow at supramaximal voltage and 25–100 Hz, in the chlorisondamine‐treated, pithed, adrenalectomized rat produced a delayed pressor response (late pressor response; LPR). 2 The LPR was abolished by phenoxybenzamine, bretylium or a small dose of atropine (25–50 μg/kg), suggesting the involvement of ganglionic muscarinic receptors. 3 In the presence of atropine at a dose level (15 μg/kg) which did not influence the LPR, the anticholinesterases physostigmine, neostigmine and Ro 02–0683 but not BW 284C51 markedly enhanced and prolonged the LPR, whereas all of them reduced the pressor responses to AHR‐602. 4 After blockade of the ganglionic muscarinic receptors with a large dose of atropine (250 μg/kg) the four anticholinesterases did not influence responses to DMPP or noradrenaline and only slightly enhanced responses to preganglionic nerve stimulation at 6 Hz in the absence of chlorisondamine. 5 It is concluded that inhibition of butyrylcholinesterase accounts for the enhancement and prolongation of the LPR by anticholinesterases.