Tomokazu Yoshida, Sayoko Mashimo, Mitsunobu Mio and Chiaki Kamei (*)
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Okayama
University, Okayama 700, Japan
(*) To whom correspondence should be addressed.
Abstract: Histamine at concentrations higher than 10-9 M significantly
elicited cortisol secretion from bovine adrenocortical (BAC) cells co-incubated
with bovine adrenal medullary (BAM) cells, suggesting that BAM cells are
responsible for histamine-induced cortisol secretion. Cortisol secretion
from BAC cells co-incubated with BAM cells was also elicited by both an
H1 agonist, 2-methylhistamine, and an H2 agonist, 4-methylhistamine. However,
4-methylhistamine was much less effective than 2-methylhistamine. Histamine-induced
cortisol secretion was inhibited not only by H1 antagonists (pyrilamine
and diphenhydramine) but also by H2 antagonists (cimetidine and ranitidine).
Histamine effectively increased 45Ca uptake and IP3 production in BAM cells.
These responses were antagonized by the H1 antagonist but not by the H2
antagonist. Histamine-induced cortisol secretion from BAC cells co-incubated
with BAM cells was inhibited by beta-adrenoceptor antagonists, propranolol
and timolol, as well as an NK1-receptor antagonist, D-Arg1-D-Trp7,9-Leu11-substance
P. These results indicate that histamine can induce cortisol secretion from
BAC cells at physiological concentrations through H1 receptors on BAM cells,
and catecholamine and substance P may participate in histamine-induced cortisol
secretion.
Keywords: Histamine, Cortisol, Bovine adrenocortical cell, Bovine adrenomedullary
cell, H1 antagonist