Francis Chaouloff, Sue H. Gunn, James B. Young
Neuroendocrinology. 1991-01-01; 54(6): 639-645
DOI: 10.1159/000125980

Lire sur PubMed

1. Neuroendocrinology. 1991 Dec;54(6):639-45.

Influence of 5-HT1 and 5-HT2 receptor antagonists on insulin-induced
adrenomedullary catecholamine release.

Chaouloff F(1), Gunn SH, Young JB.

Author information:
(1)Department of Medicine, Harvard Medical School, Boston, Mass.

Previous works have indicated that insulin stress activates the serotonin (5-HT)
and sympathoadrenal systems in the fasted rat. In addition, recent studies have
shown that activation of either the 5-HT1A, the 5-HT1C or the 5-HT2 receptor
triggers adrenal catecholamine release. Then, the aim of this study was to
investigate whether brain 5-HT, by means of these receptors, mediates
insulin-induced adrenal catecholamine release. For that purpose, both plasma
epinephrine (Epi), norepinephrine (NE) and glucose levels were measured in
conscious rats bearing intracardiac catheters. The intravenous administration of
insulin (1 IU/kg) triggered hypoglycemia throughout the following 120 min in both
fed and overnight fasted rats. Insulin stress elicited within 30 min a 5- and
38-fold increase in plasma Epi levels in fed and fasted rats, respectively. This
change was associated with significant elevations in plasma NE levels in the
fasted rats only. The intravenous administration of the mixed 5-HT1A
receptor/beta-adrenoceptor blocker (-)-propranolol (5 mg/kg) to fasted rats did
not modify plasma glucose and catecholamine peak responses to insulin; however,
at later times, insulin triggered hypoglycemic convulsions in (-)-propranolol-
but not in saline-pretreated rats. Besides, pretreatments with the 5-HT1C/5-HT2
receptor blocker LY 53857 (0.5 mg/kg), or the 5-HT1/5-HT2 receptor antagonist
metergoline (3 mg/kg), did not diminish plasma catecholamine responses to insulin
stress. Similarly, none of these antagonists affected plasma glucose recovery.
These results seem to indicate that the sympathoadrenal response to insulin
administration is not mediated by 5-HT.

DOI: 10.1159/000125980
PMID: 1784347 [Indexed for MEDLINE]

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