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Sympathetically evoked secretory potentials in the parotid gland of the cat.
Author(s) -
Emmelin N,
Grampp W,
Thesleff P
Publication year - 1980
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.1980.sp013237
Subject(s) - depolarization , chloralose , atropine , stimulation , phentolamine , guanethidine , hyperpolarization (physics) , chemistry , practolol , muscarine , medicine , endocrinology , muscarinic acetylcholine receptor , propranolol , receptor , organic chemistry , nuclear magnetic resonance spectroscopy
1. In cats under chloralose anaesthesia micro‐electrodes were inserted into parotid gland cells. 2. The average resting potential was found to be ‐35 . 6 +/‐ 4 . 7 (S.D.) mV. 3. Stimulation of the auriculo‐temporal nerve caused hyperpolarizing, or occasionally depolarizing, secretory potentials of 5‐‐10 mV, which were abolishable with atropine. 4. Stimulation of the cervical sympathetic trunk regularly caused, after long latency (several seconds), slow depolarizations of 15‐‐20 mV, accompanied by a decrease in input resistance. They were antagonized by practolol and therefore assumed to be mediated by beta 1‐adrenoceptors. Occasionally hyperpolarization, ascribed to an effect on alpha‐adrenoceptors, was observed. 5. In many units the slow depolarization on sympathetic stimulation was preceded by short‐lasting hyperpolarizing (sometimes depolarizing) transients. They resembled the evoked cholinergic responses but could be abolished not only by atropine but also by guanethidine.