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RELEASE OF NORADRENALINE FROM CAT SPLEEN SLICES BY POTASSIUM
Author(s) -
GARCÍA A.G.,
KIRPEKAR S.M.,
PASCUAL R.
Publication year - 1978
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.1476-5381.1978.tb08447.x
Subject(s) - phenoxybenzamine , phentolamine , chemistry , potassium , depolarization , phenylephrine , endocrinology , acetylcholine , medicine , stimulation , sodium , prazosin , pharmacology , receptor , biochemistry , antagonist , organic chemistry , blood pressure
1 When cat spleen slices were exposed to a potassium‐enriched (140mM) Krebs solution, 367 ± 31 ng g −1 5 min −1 of noradrenaline (NA) was released into the bathing medium. 2 Phenylephrine and clonidine (10 −7 to 10 −3 M) did not significantly modify the potassium‐evoked NA release; acetylcholine decreased it in a dose‐dependent manner. 3 Phenoxybenzamine increased NA release by 50% but phentolamine did not alter it; high concentrations of this drug greatly decreased NA release. Cocaine increased the NA release by about 30%. 4 It is suggested that the failure of sympathomimetic amines to depress, and of α‐adrenoceptor blocking agents to enhance the release of NA by high potassium concentrations may be related to prolonged depolarization of the nerve terminals, which may desensitize presynaptic α‐receptors. The fact that the same drugs are able to modify NA release during electrical nerve stimulation may be ascribed to the much shorter periods of depolarization occurring under these conditions.