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Inhibitory muscarinic receptors and α‐adrenoceptors on cholinergic axon terminals in the urethra of rabbit and man
Author(s) -
Mattiasson Anders,
Andersson KarlErik,
Sjögren Christer
Publication year - 1987
Publication title -
neurourology and urodynamics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 90
eISSN - 1520-6777
pISSN - 0733-2467
DOI - 10.1002/nau.1930060604
Subject(s) - phentolamine , hexamethonium , cholinergic , muscarinic acetylcholine receptor , carbachol , muscarine , endocrinology , medicine , adrenergic , rauwolscine , agonist , axon , stimulation , receptor , prazosin , anatomy , antagonist
Isolated smooth‐muscle preparations from the rabbit and human urethra were incubated with 3 H‐choline, and the influence of drugs on the electrically induced release of 3 H was studied. In both rabbit and human urethral smooth muscle, the release was well reproducible and abolished in the presence of tetrodotoxin, indicating a nervous origin. By means of drugs stimulating (carbachol, nicotine amide) and blocking (scopolamine, hexamethonium) cholinoceptors, release‐inhibiting muscarinic but not nicotinic receptors could be demonstrated on the cholinergic axon terminals. The stimulation‐induced efflux of 3 H was significantly and concentration‐dependently inhibited by noradrenaline (NA) and the selective α 2 ‐adrenoceptor agonist, clonidine. The effects of NA and clonidine were abolished by phentolamine. Phentolamine by itself did not influence the release, nor did rauwolscine. Morphological investigations have revealed close contacts between adrenergic and cholinergic axon terminals, and the occurrence of muscarinic receptors on adrenergic axon terminals inhibiting release of NA in the urethra has previously been demonstrated. The present results therefore suggest the possibility of a mutual interaction between adrenergic and cholinergic neurons at the axon‐terminal level in the urethra.