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alpha‐Adrenergic, beta‐adrenergic and cholinergic mechanisms for amylase secretion by rat parotid gland in vitro.
Author(s) -
Leslie B A,
Putney J W,
Sherman J M
Publication year - 1976
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1976.sp011519
Subject(s) - isoprenaline , endocrinology , medicine , cholinergic , exocytosis , secretion , purinergic receptor , stimulation , adrenergic , agonist , chemistry , extracellular , adrenergic receptor , cyclic nucleotide , second messenger system , receptor , biology , adenosine , microbiology and biotechnology , biochemistry , nucleotide , gene
1. Rat parotid gland slices, incubated in a balanced, buffered salt solution, were found to be physiologically stable for up to 2 hr with respect to O2 consumption, water content, extracellular space and cation content. 2. The slices could be stimulated to secrete amylase by activation of alpha‐adrenergic, beta‐adrenergic or muscarinic cholinergic receptors. 3. The secretion elicited through all three receptors appeared to involve exocytosis as revealed by electron microscopy. 4. The beta‐agonist, isoprenaline, increased tissue content of cyclic adenosine 3',5'‐monophosphate (cyclic AMP); alpha‐adrenergic and cholinergic agents had no effect on the level of this cyclic nucleotide. 5. Secretion via cholinergic or alpha‐adrenergic mechanisms required extra‐cellular calcium; the beta‐adrenergic mechanism did not. 6. It was concluded that stimulation of rat parotid cells activates distinctly separate pathways leading ultimately to exocytosis, one pathway involving cyclic AMP, and the other, external Ca2+ ion.