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Possible involvement of glucocorticoids in the modulation of interleukin‐1‐induced cardiovascular responses in rats.
Author(s) -
Watanabe T,
Tan N,
Saiki Y,
Makisumi T,
Nakamura S
Publication year - 1996
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.1996.sp021211
Subject(s) - medicine , endocrinology , corticosterone , adrenalectomy , glucocorticoid , dexamethasone , heart rate , microgram , beta (programming language) , chemistry , blood pressure , hormone , in vitro , biochemistry , computer science , programming language
1. In freely moving rats, we investigated whether glucocorticoids modulate the cardiovascular responses to intraperitoneal (I.P.) injection of interleukin‐1 beta (IL‐1 beta). 2. A lower dose of IL‐1 beta (1 microgram kg‐1, I.P.) induced monophasic increases, and a higher dose (10 micrograms kg‐1, I.P.) induced biphasic increases in both blood pressure and heart rate. Plasma concentration of corticosterone increased significantly after injection of IL‐1 beta (10 micrograms kg‐1). 3. Systemic pretreatment with an exogenous glucocorticoid, dexamethasone (DEX; 0.5 mg kg‐1) reduced the monophasic pressor response, the first phase of the biphasic pressor response and also the initial tachycardia. By contrast, the second phase of the biphasic pressor response was enhanced. 4. After bilateral adrenalectomy, the IL‐1 beta (10 micrograms kg‐1)‐induced pressor effect was reduced; it was restored by treatment with DEX (0.5 mg kg‐1). The heart rate response was enhanced in adrenalectomized (ADX) rats; this enhancement was attenuated by DEX. 5. IL‐1 beta (10 micrograms kg‐1)‐induced increases in plasma noradrenaline (NA) were suppressed in intact rats pretreated with DEX (0.5 mg kg‐1). The IL‐1 beta‐induced NA response was greater in ADX rats than in sham‐ADX rats. 6. We suggest that glucocorticoids are an important modulator of cardiovascular responses induced in rats by systemically administered IL‐1 beta.