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Voltage‐independent catecholamine release mediated by the activation of muscarinic receptors in guinea‐pig adrenal glands
Author(s) -
Nakazato Y.,
Ohga A.,
Oleshansky M.,
Tomita U.,
Yamada Y.
Publication year - 1988
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.1476-5381.1988.tb11410.x
Subject(s) - muscarinic acetylcholine receptor , catecholamine , guinea pig , endocrinology , medicine , receptor , adrenal gland , adrenal medulla , biology , chemistry
1 The differences between the mechanisms of muscarinic and nicotinic receptor‐mediated catecholamine secretion with respect to their dependence on voltage changes and extracellular Ca were examined using perfused adrenal glands of the guinea‐pig. 2 Acetylcholine (ACh, 10 −6 to 10 −3 m ) caused a dose‐dependent increase in catecholamine secretion. The ED 50 value for ACh was 7 × 10 −5 m . In the presence of atropine (10 −5 m ), the dose‐response curve for ACh was shifted to the right. Hexamethonium (5 × 10 −4 m ) preferentially reduced the responses to higher concentrations of ACh (> 10 −5 m ). Pilocarpine (5 × 10 −4 m ) and nicotine (3 × 10 −5 m ) also stimulated catecholamine release. 3 During perfusion with isotonic KCl solution, ACh and pilocarpine, but not nicotine, evoked catecholamine secretion. These responses were abolished by atropine (10 −6 m ). Pilocarpine‐stimulated catecholamine secretion was enhanced during perfusion with isotonic KCl solution. Under these conditions, hexamethonium (10 −3 m ) significantly augmented ACh‐evoked catecholamine release. 4 During perfusion with either Ca‐free isotonic KCl or Ca‐free Locke solution, ACh and pilocarpine caused a partial increase in catecholamine secretion whereas nicotine and high K solution (56 m m ) did not. The responses to ACh and pilocarpine were completely inhibited by atropine but not by hexamethonium. 5 When guinea‐pig adrenal glands were perfused with isotonic KCl solution containing 2.2 m m Ca which was subsequently removed and replaced with EGTA, ACh‐induced catecholamine secretion was similar in magnitude to that observed during perfusion with Locke solution. 6 We conclude that both nicotinic and muscarinic receptors are involved in ACh‐induced catecholamine secretion from guinea‐pig adrenal chromaffin cells. Activation of muscarinic or nicotinic receptors appears to stimulate catecholamine release through different mechanisms with respect to both voltage‐dependence and Ca requirements.