Activation of sympathetic outflow by recombinant human interleukin-1 beta in conscious rats

1996 ◽  
Vol 270 (2) ◽  
pp. R479-R485 ◽  
Author(s):  
H. Kannan ◽  
Y. Tanaka ◽  
T. Kunitake ◽  
Y. Ueta ◽  
Y. Hayashida ◽  
...  
Keyword(s):  
Body Temperature ◽  
Prostaglandin E2 ◽  
Interleukin 1 ◽  
Plasma Norepinephrine ◽  
Intracerebroventricular Injection ◽  
Sympathetic Outflow ◽  
Interleukin 1 Beta ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Intracerebroventricular Injections

The present study was undertaken to determine the effects of interleukin-1 beta (IL-1 beta) on renal sympathetic nerve activity (RSNA), arterial blood pressure (AP), heart rate (HR), and body temperature in conscious rats. Either intravenous or intracerebroventricular administration of IL-1 beta elicited increases in AP, HR, and RSNA accompanied by a rise in body temperature. The maximum changes in AP, HR, and RSNA occurred 10-15 min after intravenous injection of IL-1 beta (100 ng) and 20-25 min after intracerebroventricular injection (5 ng). The responses induced by the intravenous and intracerebroventricular injections lasted for approximately 15-30 min and did not appear when the animals were pretreated with the cyclooxygenase inhibitor indomethacin (10 mg/kg iv). Moreover, intracerebroventricular injection of prostaglandin E2 (1 microgram) produced responses similar to those induced by IL-1 but with shorter latency. Plasma norepinephrine and adrenocorticotropic hormone concentrations were increased after IL-1 beta injection. The results suggested that IL-1 beta augments cardiovascular and sympathetic outflow through the central action of prostaglandin E2 in conscious rats.

Stereoselective actions of S-nitrosocysteine in central nervous system of conscious rats

1997 ◽  
Vol 272 (5) ◽  
pp. H2361-H2368 ◽  
Author(s):  
R. L. Davisson ◽  
M. D. Travis ◽  
J. N. Bates ◽  
A. K. Johnson ◽  
S. J. Lewis
Keyword(s):  
Central Nervous System ◽  
Heart Rate ◽  
Nervous System ◽  
Intracerebroventricular Injection ◽  
Conscious Rats ◽  
Arterial Blood ◽  
Recognition Sites ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Intracerebroventricular Injections

This study examined whether the stereoselective actions of S-nitrosocysteine (SNC) in the central nervous system involves the activation of stereoselective SNC recognition sites. We examined the effects produced by intracerebroventricular injection of the L- and D-isomers of SNC (L- and D-SNC) on mean arterial blood pressure, heart rate, and vascular resistances in conscious rats. We also examined the hemodynamic effects produced by intracerebroventricular injections of 1) L-cystine, the major non-nitric oxide (NO) decomposition product of L-SNC, 2) the parent thiols L- and D-cysteine, and 3) the bulky S-nitrosothiol L-S-nitroso-gamma-glutamylcysteinylglycine [L-S-nitrosoglutathione, (L-SNOG)]. Finally, we examined the decomposition of L- and D-SNC and L-SNOG to NO on their addition to brain homogenates. The intracerebroventricular injection of L-SNC (250-1,000 nmol) produced falls in mean arterial pressure, increases in heart rate, and a dose-dependent pattern of changes in hindquarter, renal, and mesenteric vascular resistances. The intracerebroventricular injections of D-SNC, L-cystine, and L-SNOG produced only minor effects. The intracerebroventricular injection of L-cysteine produced pressor responses and tachycardia, whereas D-cysteine was inactive. L- and D-SNC decomposed equally to NO on addition to brain homogenates. L-SNOG decomposed to similar amounts of NO as L- and D-SNC. These results suggest that SNC may activate stereoselective SNC recognition sites on brain neurons and that S-nitrosothiols of substantially different structure do not stimulate these sites. These recognition sites may be stereoselective membrane-bound receptors for which L-SNC is the unique ligand.

Interleukin-8 induces fever by a prostaglandin-independent mechanism

1994 ◽  
Vol 266 (5) ◽  
pp. R1670-R1674 ◽  
Author(s):  
A. R. Zampronio ◽  
G. E. Souza ◽  
C. A. Silva ◽  
F. Q. Cunha ◽  
S. H. Ferreira
Keyword(s):  
Body Temperature ◽  
Interleukin 1 ◽  
Interleukin 8 ◽  
Cyclooxygenase Inhibitors ◽  
Interleukin 1 Beta ◽  
Independent Mechanism ◽  
Intracerebroventricular Injections ◽  
Beta 2 ◽  
Dose Dependent ◽  
Pyrogenic Activity

We have studied the mechanism by which interleukin-8 (IL-8) induces fever in rats. Intracerebroventricular injections of IL-8 (5.5-50 ng) evoked dose-dependent increases in body temperature, which reached a plateau 5 h after injection, i.e., later than intracerebroventricular interleukin-1 beta (IL-1 beta; 2 h). The pyrogenic activity of IL-8 was not due to contamination with lipopolysaccharide (LPS) because preincubation of IL-8 with a specific antibody or boiling the IL-8 for 30 min abolished its activity but not that of LPS; also, IL-8 but not LPS induced fever in LPS-tolerant rats. Indomethacin significantly reduced the pyrogenic effects of intracerebroventricular injections of LPS and IL-1 beta but not responses to IL-8, suggesting that pyrogenic responses to IL-8 were mediated independently of prostaglandins. In contrast, dexamethasone markedly attenuated pyrogenic responses to IL-8 and IL-1 beta. These data suggest that inhibition of IL-8 by glucocorticoids contributes to the antipyretic effects of these drugs in fevers resistant to cyclooxygenase inhibitors.

scholarly journals Febrile responses induced in adrenalectomized rats by administration of interleukin-1 beta or prostaglandin E2.

1995 ◽  
Vol 484 (3) ◽  
pp. 767-775 ◽  
Author(s):  
T Watanabe ◽  
T Makisumi ◽  
M Macari ◽  
N Tan ◽  
T Nakamori ◽  
...  
Keyword(s):  
Prostaglandin E2 ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Adrenalectomized Rats

Hypothalamic neuronal histamine modulates physiological responses induced by interleukin-1 beta

1995 ◽  
Vol 269 (6) ◽  
pp. R1308-R1313 ◽  
Author(s):  
M. Kang ◽  
H. Yoshimatsu ◽  
S. Chiba ◽  
M. Kurokawa ◽  
R. Ogawa ◽  
...  
Keyword(s):  
Body Temperature ◽  
Intraperitoneal Injection ◽  
Histidine Decarboxylase ◽  
Interleukin 1 ◽  
Suppressive Effect ◽  
Ingestive Behavior ◽  
Interleukin 1 Beta ◽  
Hypothalamic Histamine ◽  
Food And Water Intake ◽  
Neuronal Histamine

Dynamic involvement of hypothalamic histamine in ingestive behavior and thermogenesis induced by interleukin-1 beta (IL-1 beta) was examined in rats. Intraperitoneal injection of 0.12 nmol/rat IL-1 beta decreased food and water intake and elevated body temperature. However, depletion of neuronal histamine induced by intraperitoneal injection of 160 mumol/rat alpha-fluoromethylhistidine, a suicide inhibitor of histidine decarboxylase (HDC), attenuated the suppressive effect of IL-1 beta on food intake, facilitated the suppressive effect on drinking, and enhanced the elevating effect on rectal temperature. Intraperitoneal injection of 0.12 nmol/rat IL-1 beta increased hypothalamic histamine turnover rate. The same dose of IL-1 beta also increased activity of HDC and histamine-N-methyltransferase (HMT). These results suggest that IL-1 beta may stimulate synthesis and release of hypothalamic histamine in presynaptic terminals by activation of HDC and facilitate degradation of extracellular histamine by activation of MHT. These changes in the dynamics of hypothalamic histamine modulate IL-1 beta-induced ingestive behavior and body temperature.

Cardiovascular effects of human recombinant interleukin-1 beta in conscious rats

1994 ◽  
Vol 266 (4) ◽  
pp. R1148-R1153 ◽  
Author(s):  
A. Bataillard ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Enzyme Inhibitor ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Interleukin 1 ◽  
Renin Angiotensin System ◽  
Cardiovascular Effects ◽  
Interleukin 1 Beta ◽  
Pronounced Increase ◽  
Arterial Blood

Cardiovascular effects of human recombinant interleukin-1 beta (hrIL-1 beta) were investigated in normotensive rats using a computerized analysis of arterial blood pressure in conscious, unrestrained animals. Intravenous injection of hrIL-1 beta induced a rapid and short-lasting rise in blood pressure associated with a first slight tachycardia followed by a second sustained and pronounced increase in heart rate. These effects occurred in a dose-related manner. Pretreatment with a converting-enzyme inhibitor (perindopril) did not modify the hrIL-1 beta-induced increase in blood pressure. Blockade of beta 1-adrenoceptors (atenolol) prevented the tachycardia, but did not significantly affect the pressor response to hrIL-1 beta. On the contrary, the hrIL-1 beta-induced increase in blood pressure was inhibited by an alpha 1-adrenoceptor antagonist (prazosin), whereas the tachycardia was untouched. Finally, pretreatment with a cyclooxygenase inhibitor (indomethacin) completely abolished the cardiovascular response to hrIL-1 beta. These results suggest that the hrIL-1 beta-induced pressor response and associated tachycardia require the synthesis of prostaglandins and involve a sympathetic nervous system activation but do not depend on the renin-angiotensin system.

Lipocortin 1 fragment modifies pyrogenic actions of cytokines in rats

1990 ◽  
Vol 259 (2) ◽  
pp. R266-R269 ◽  
Author(s):  
F. Carey ◽  
R. Forder ◽  
M. D. Edge ◽  
A. R. Greene ◽  
M. A. Horan ◽  
...  
Keyword(s):  
Heat Treatment ◽  
Interleukin 1 ◽  
Physiological Role ◽  
Polyclonal Antiserum ◽  
Intracerebroventricular Injection ◽  
Interleukin 1 Beta ◽  
Recombinant Fragment ◽  
Central Effects ◽  
Colonic Temperature ◽  
Dose Dependent

Lipocortins form a group of proteins that have been proposed as mediators of the anti-inflammatory actions of glucocorticoids. Intracerebroventricular injection of a recombinant fragment of lipocortin 1 (NH2-terminal 1-188) caused dose-dependent (0.4-1.2 micrograms) reductions in the acute increases in colonic temperature and oxygen consumption, which occurred in response to central injections of recombinant interleukin 1 beta and gamma-interferon in conscious rats. In contrast the lipocortin fragment did not affect the response to prostaglandin E2, and its activity was prevented by heat treatment or by pretreatment of animals with polyclonal antiserum raised to the fragment. Central injection of antiserum significantly enhanced the thermogenic responses to interleukin 1 beta in rats treated with dexamethasone without affecting the responses in normal animals. These results support a physiological role for lipocortin in the central effects of glucocorticoids.

Importance of brain IL-1 type II receptors in fever and thermogenesis in the rat

1993 ◽  
Vol 265 (4) ◽  
pp. E585-E591 ◽  
Author(s):  
G. Luheshi ◽  
S. J. Hopkins ◽  
R. A. Lefeuvre ◽  
M. J. Dascombe ◽  
P. Ghiara ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Low Dose ◽  
Interleukin 1 ◽  
Type I ◽  
Intracerebroventricular Injection ◽  
Type Ii ◽  
Central Effects ◽  
Conscious Rats ◽  
Central Actions ◽  
The Brain

Interleukin-1 (IL-1) acts centrally to induce fever and thermogenesis in rodents. The central actions of IL-1 alpha and IL-1 beta apparently involve different mechanisms, and the effects of IL-1 beta are not consistent with interaction with a type I (IL-1RI) 80-kDa receptor. In the present study the involvement of the type II IL-1 receptor (IL-1RII) was tested in the rat by examining the effects of central injection of a monoclonal antibody (ALVA-42), which blocks the IL-1RII. Pretreatment of rats with ALVA-42 (6 micrograms icv) inhibited the thermogenic and pyrogenic responses to intracerebroventricular injection of 5 ng (but not 50 ng) of IL-1 beta in conscious rats but did not significantly modify responses to IL-1 alpha. ALVA-42 also failed to modify the responses to peripherally administered IL-1 beta (1 microgram) but significantly attenuated the pyrogenic and thermogenic responses to peripheral (125 micrograms) or central (1 microgram) injection of endotoxin. These data indicate that IL-1RII mediates the central effects of a low dose of IL-1 beta, but not IL-1 alpha, on fever and thermogenesis in the rat. They also imply that responses to endotoxin are due, at least in part, to the activation of IL-1RII by IL-1 beta released within the brain and that effects of peripherally injected IL-1 beta involve different mechanisms, probably associated with IL-1RI.

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