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22 Na + Uptake and Catecholamine Secretion by Primary Cultures of Adrenal Medulla Cells
Author(s) -
Amy Christopher,
Kirshner Norman
Publication year - 1982
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1982.tb04711.x
Subject(s) - veratridine , adrenal medulla , catecholamine , medicine , endocrinology , chromaffin cell , tetrodotoxin , chemistry , ionomycin , secretion , acetylcholine , biology , sodium , stimulation , sodium channel , organic chemistry
The uptake of 22 Na + and secretion of catecholamines by primary cultures of adrenal medulla cells under the influence of a variety of agonists and antagonists were determined. Veratridine, batrachotoxin, scorpion venom, and nicotine caused a parallel increase in 22 Na + uptake and Ca 2+ –dependent catecholamine secretion. Ba 2+ , depolarizing concentrations of K + , and the Ca 2+ ionophore Ionomycin stimulated secretion of catecholamines but did not increase the uptake of 22 Na + . Tetrodotoxin inhibited both 22 Na + uptake and catecholamine secretion evoked by veratridine, batrachotoxin, and scorpion venom, but had no effect on 22 Na + uptake and catecholamine secretion caused by nicotine. On the other hand, histrionicotoxin, which blocks the acetylcholine receptor–linked ion conductance channel, blocked nicotine–stimulated 22 Na + uptake and catecholamine secretion, but only partially inhibited veratridine–stimulated catecholamine secretion and had no effect on veratridine–stimulated 22 Na + uptake. The combination of veratridine plus tetrodotoxin, which has been shown to prevent nicotine–stimulated secretion of catecholamines by adrenal medulla cells, also prevented nicotine–stimulated 22 Na + uptake by the primary cultures. These studies demonstrate the presence of tetrodotoxin–sensitive Na + channels in adrenal medulla cells which are functionally linked to Ca 2+ –dependent catecholamine secretion. However, these channels are not utilized for Na + entry upon activation of nicotinic receptors; in this case Na + entry occurs through the receptor‐associated ion conductance channel.