A COMPARISON OF THE EFFECTS OF REPEATED STRESSOR EXPOSURES AND CORTICOSTERONE INJECTIONS ON PLASMA-CHOLESTEROL, THYROID-HORMONES AND CORTICOSTERONE LEVELS IN RATS
Rj. Servatius et al., A COMPARISON OF THE EFFECTS OF REPEATED STRESSOR EXPOSURES AND CORTICOSTERONE INJECTIONS ON PLASMA-CHOLESTEROL, THYROID-HORMONES AND CORTICOSTERONE LEVELS IN RATS, Life sciences, 55(21), 1994, pp. 1611-1617
Citations number
21
Categorie Soggetti
Biology,"Medicine, Research & Experimental","Pharmacology & Pharmacy
Persistently elevated serum cholesterol (CHOL) levels have been observ
ed in rats given repeated stressor exposures and fed a normal laborato
ry diet. To determine the relative contribution of persistent hormone
changes in the hypothalamic-pituitary-adrenal (HPAA) and thyroid axes
to persistent stress-induced CHOL elevations, the present experiment a
ssessed the contribution of persistently elevated corticosterone (CORT
) from both endogenous and exogenous sources. Groups of rats were expo
sed for 7 days to stress sessions (7DS; 40, 2mA tailshocks given over
2 h each day), CORT injections (CI; 10 mg/1 ml vehicle/day) or vehicle
injections (VI; sesame oil), or served as noninjected, undisturbed co
ntrols(CON). In addition, another group of rats were adrenalectomized
(ADX). Basal blood samples were drawn for CORT determination on the 1s
t, 4th, 7th, and 8th experimental days. The blood samples from the 8th
day, 22 h after the last stress session or injection were also assaye
d for CHOL, T3 and T4. The basal CORT levels of both 7DS and CI rats w
ere elevated on the 4th and 7th experimental days. Contrary to expecta
tions, 7 daily exposures to the stress regimen did not persistently al
ter plasma CORT, CHOL, T3 or T4 levels. The CI rats did exhibit elevat
ed CORT on the 8th experimental day which was accompanied by elevated
CHOL levels and suppressed T4 levels. However, elevated CHOL levels we
re also found in ADX rats and these elevations were accompanied by sup
pressed T3 levels. These data suggest that persistent CORT elevations
are not necessary for persistent plasma CHOL elevations after stressor
exposure, but further research is necessary to clarify the role of th
e HPAA and thyroid axes in stress-induced plasma CHOL elevations.