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Association of the Serum Angiotensin II Level with Disease Severity in Severe Fever with Thrombocytopenia Syndrome Patients.

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OBJECTIVE Severe fever with thrombocytopenia syndrome (SFTS) is an emerging infectious disease caused by a novel Bunyavirus. Recent data suggest that the physiological balance of multiple proinflammatory cytokines is substantially changed in cases of severe fever with thrombocytopenia syndrome virus

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.

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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

Angiotensin-converting enzyme inhibitor inhibits dehydration-enhanced fever induced by endotoxin in rats.

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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.

Angiotensin-converting enzyme genotype predicts valve damage in acute rheumatic fever.

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OBJECTIVE The genetic basis for host susceptibility to subsequent valve damage and scarring is not well defined in patients with a history of acute rheumatic fever (ARF). A high angiotensin-converting enzyme (ACE) activity has been demonstrated in valve tissue; hence, the study aim was to determine

The effect of central angiotensin II receptor blockade on interleukin-1beta- and prostaglandin E-induced fevers in rats: possible involvement of brain angiotensin II receptor in fever induction.

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We investigated the role of the brain angiotensin II (Ang II) receptor subtypes AT1 and AT2 in the development of fever induced in freely moving rats by administration of interleukin-1beta (IL-1beta) or prostaglandin E2 (PGE2). Intraperitoneal (i.p.) injection of IL-1beta (2 microg/kg) induced a

Angiotensin II: its effects on fever and hypothermia in systemic inflammation.

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Angiotensin II (ANG II), a bioactive peptide that plays important roles in blood-pressure and body-fluid regulation, has recently been reported to be involved in normal thermoregulation and fever. In the case of thermoregulation, ANG II lowers body temperature when administered centrally or

Hyperthermia treatment prevents angiotensin II-mediated atrial fibrosis and fibrillation via induction of heat-shock protein 72.

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We tested the hypothesis that atrial fibrosis and atrial fibrillation (AF) evoked by angiotensin II (AII) could be prevented by the induction of heat-shock protein 72 (HSP72) by hyperthermia (HT). In cultured atrial fibroblasts isolated from male Sprague-Dawley rats, HT (42 degrees C) was applied

Effects of targeted disruption of the mouse angiotensin II type 2 receptor gene on stress-induced hyperthermia.

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1. We have previously reported that brain angiotensin II type 2 receptors (AT2) contribute to immunological stress-induced hyperthermia (fever) in rats. Now, in mice, we report the effect of AT2 gene disruption on the hyperthermia induced by immunological (interleukin-1 (IL-1) injection) and

The effect of angiotensin II on blood flow in tumours during localized hyperthermia.

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The selective enhancement of drug delivery to tumours is an important factor in the effectiveness of thermochemotherapy as well as in standard normothermal chemotherapy. We have attempted to clarify experimentally using AH 100B tumour-bearing rats whether or not a selective increase in blood flow in

Hsp70 does not mediate the hyperthermia-associated hyporesponsiveness to angiotensin in isolated rat portal veins.

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In rat portal veins (RPV) isolated from septic rats, we previously showed that the contractile response to angiotensin II (AT(II)) was significantly decreased and that the vascular failure was correlated with the severity of the disease. We hypothesized that hyperthermia might be one of the factors

Angiotensin Converting Enzyme Gene Insertion/Deletion Variant and Familial Mediterranean Fever-related Amyloidosis.

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The most important complication of familial Mediterranean fever (FMF) is secondary amyloidosis, which can lead to kidney failure. Genetic variability in the genes of various components of the renin-angiotensin system may play a role in the pathogenesis of the kidney disorders. The aim of the

Vasopressor responses and hyperthermia by intracerebroventricular injections of penicillin, a pyrogen, in rats: involvement of brain angiotensin II.

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Because hypothalamus is a center for both the blood pressure and thermoregulation, we assumed that there is a close interrelationship between them. To prove this hypothesis, effects of intracerebroventricular (ICV) injections of a pyrogen, penicillin-G (Pc), on the blood pressure and rectal

[A study on the changes in renin-angiotensin-aldosterone system in epidemic hemorrhagic fever and their clinical significance].

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Familial Mediterranean fever. Another cause of raised serum angiotensin converting enzyme; another abortive attempt at masquerading as sarcoidosis.

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Angiotensin converting enzyme estimation in pyrexia of unknown origin with bilateral hilar lymphadenopathy--an essential investigation.

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