Possible involvement of glucocorticoids in the modulation of interleukin-1-induced cardiovascular responses in rats

被引:16
作者
Watanabe, T
Tan, N
Saiki, Y
Makisumi, T
Nakamura, S
机构
[1] Department of Physiology, Yamaguchi University, School of Medicine
来源
JOURNAL OF PHYSIOLOGY-LONDON | 1996年 / 491卷 / 01期
关键词
D O I
10.1113/jphysiol.1996.sp021211
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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 mu g kg(-1), I.P.) induced monophasic increases, and a higher dose (10 mu g 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 mu g kg(-1)). 3. Systemic pretreatment with an exogenous glucocorticoid, dexamethasone (DEX; 0.5 mg kg(-1)) reduced the monophasic presser response, the first phase of the biphasic presser response and also the initial tachycardia. By contrast, the second phase of the biphasic presser response was enhanced. 4. After bilateral adrenalectomy, the IL-1 beta (10 mu g kg(-1))-induced presser 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 mu g 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.
引用
收藏
页码:231 / 239
页数:9
相关论文
共 29 条
[1]  
BATAILLARD A, 1992, AM J PHYSIOL, V263, pR884
[2]  
BATAILLARD A, 1994, AM J PHYSIOL, V35, pR1148
[3]  
BAXTER JD, 1979, GLUCOCORTICOID HORMO, P1
[4]   NEURO-ENDOCRINE, SYMPATHETIC AND METABOLIC RESPONSES INDUCED BY INTERLEUKIN-1 [J].
BERKENBOSCH, F ;
DEGOEIJ, DEC ;
DELREY, A ;
BESEDOVSKY, HO .
NEUROENDOCRINOLOGY, 1989, 50 (05) :570-576
[5]   IMMUNOREGULATORY FEEDBACK BETWEEN INTERLEUKIN-1 AND GLUCOCORTICOID HORMONES [J].
BESEDOVSKY, H ;
DELREY, A ;
SORKIN, E ;
DINARELLO, CA .
SCIENCE, 1986, 233 (4764) :652-654
[6]  
BROWN MR, 1985, FED PROC, V44, P243
[7]   A STUDY OF THE PYROGENIC ACTIONS OF INTERLEUKIN-1-ALPHA AND INTERLEUKIN-1-BETA - INTERACTIONS WITH A STEROIDAL AND A NONSTEROIDAL ANTIINFLAMMATORY AGENT [J].
DAVIDSON, J ;
MILTON, AS ;
ROTONDO, D .
BRITISH JOURNAL OF PHARMACOLOGY, 1990, 100 (03) :542-546
[8]   AUTONOMIC AND BEHAVIORAL-EFFECTS OF CENTRALLY ADMINISTERED CORTICOTROPIN-RELEASING FACTOR IN RATS [J].
DIAMANT, M ;
DEWIED, D .
ENDOCRINOLOGY, 1991, 129 (01) :446-454
[9]   INTERLEUKIN-1 [J].
DINARELLO, CA .
REVIEWS OF INFECTIOUS DISEASES, 1984, 6 (01) :51-95
[10]   HYPOTHALAMIC SITES FOR CARDIOVASCULAR AND SYMPATHETIC MODULATION BY PROSTAGLANDIN-E2 [J].
FEUERSTEIN, G ;
ADELBERG, SA ;
KOPIN, IJ ;
JACOBOWITZ, DM .
BRAIN RESEARCH, 1982, 231 (02) :335-342