lisinopril has been researched along with Fever* in 3 studies
3 other study(ies) available for lisinopril and Fever
Article | Year |
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Chest pain · shortness of breath · fever and nausea · Dx?
Topics: Adult; Antihypertensive Agents; Chest Pain; Diagnosis, Differential; Diuretics; Electrocardiography; Fever; Furosemide; Humans; Lisinopril; Male; Metoprolol; Myocardial Infarction; Myocarditis; Stroke Volume; Systemic Inflammatory Response Syndrome; Treatment Outcome; Troponin I; West Nile Fever; West Nile virus | 2015 |
The effect of central injection of angiotensin-converting enzyme inhibitor and the angiotensin type 1 receptor antagonist on the induction by lipopolysaccharide of fever and brain interleukin-1beta response in rats.
We recently reported an involvement of peripheral angiotensin II (ANG II) in the development of both the fever and the peripheral interleukin (IL)-1beta production induced in rats by a systemic injection of lipopolysaccharide (LPS). The present study was performed to investigate whether brain ANG II contributes to the fever and IL-1beta production in the rat brain induced by i.c.v. injection of LPS. LPS (0.2 and 2 microg i.c.v.) induced dose-related fevers and increases in the brain (hypothalamus, hippocampus, and cerebellum) concentrations of IL-1beta. These effects were significantly inhibited by i.c.v. administration of either an angiotensin-converting-enzyme (ACE) inhibitor or an angiotensin type 1 (AT(1)) receptor antagonist. By contrast, the ACE inhibitor had no effect on the IL-1beta (i.c.v.)-induced fever, whereas the AT(1) receptor antagonist enhanced (rather than reduced) it. The AT(1) receptor antagonist had no effect on the brain levels of prostaglandin E(2) in rats given an i.c.v. injection of IL-1beta. These results suggest that in rats, brain ANG II and AT(1) receptors are involved in the LPS-induced production of brain IL-1beta, thus contributing to the fever induced by the presence of LPS within the brain. Topics: Angiotensin II Type 1 Receptor Blockers; Angiotensin-Converting Enzyme Inhibitors; Angiotensins; Animals; Antihypertensive Agents; Brain; Disease Models, Animal; Fever; Injections; Interleukin-1; Lipopolysaccharides; Lisinopril; Losartan; Male; Rats; Rats, Wistar | 2004 |
Angiotensin-converting enzyme inhibitor inhibits dehydration-enhanced fever induced by endotoxin in rats.
It has been reported that a host develops a marked fever under dehydrated conditions compared with normally hydrated conditions (11). The present study was carried out to investigate whether ANG II is involved in the enhancement seen in dehydrated rats of the fever induced by bacterial endotoxin. The results showed that intravenous injection of bacterial endotoxin produced a fever in dehydrated rats (rats deprived of water for 24 h) that was significantly greater than that seen in normally hydrated rats. In contrast, dehydration had no effect on the fever induced by intravenous interleukin-1beta (IL-1beta). Under dehydrated conditions, the enhanced endotoxin-induced fever was significantly inhibited by the angiotensin-converting enzyme inhibitor lisinopril, but the IL-1beta fever was not. These results suggest that the dehydration-induced enhancement of endotoxin fever is due, at least in part, to the action of ANG II, which elicits an increased production of pyrogenic cytokines such as IL-1. Topics: Analysis of Variance; Angiotensin-Converting Enzyme Inhibitors; Animals; Dehydration; Endotoxins; Fever; Humans; Interleukin-1; Lipopolysaccharides; Lisinopril; Male; Rats; Rats, Wistar; Recombinant Proteins; Salmonella typhi | 2000 |