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

Kannan, Hiroshi; Tanaka, Yuta; Kunitake, Takato; Ueta, Y.; Hayashida, Yoshiaki; Yamashita, Haruyo

doi:10.1152/ajpregu.1996.270.2.r479

Cited by 45 publications

(44 citation statements)

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“…Fg is synthesized and assembled in hepatocytes and fibroblasts, and when secreted into the circulation, has a plasma half-life that ranges from 3 days to 4 days [12]. Synthesis of Fg involves other inflammatory mediators such as interleukin (IL)-6 and IL-1 [13,14], which like Fg, are associated with elevation of blood pressure [15][16][17] and development of hypertension [15,18,19], respectively.…”

Section: Introductionmentioning

confidence: 99%

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Fibrinogen induces endothelial cell permeability

et al. 2007

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Many cardiovascular and cerebrovascular disorders are accompanied by an increased blood content of fibrinogen (Fg), a high molecular weight plasma adhesion protein. Fg is a biomarker of inflammation and its degradation products have been associated with microvascular leakage. We tested the hypothesis that at pathologically high levels, Fg increases endothelial cell (EC) permeability through extracellular signal regulated kinase (ERK) signaling and by inducing F-actin formation. In cultured ECs, Fg binding to intercellular adhesion molecule-1 and to α 5 β 1 integrin, caused phosphorylation of ERK. Subsequently, F-actin formation increased and coincided with formation of gaps between ECs, which corresponded with increased permeability of ECs to albumin. Our data suggest that formation of F-actin and gaps may be the mechanism for increased albumin leakage through the EC monolayer. The present study indicates that elevated un-degraded Fg may be a factor causing microvascular permeability that typically accompanies cardiovascular and cerebrovascular disorders.

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Section: Introductionmentioning

confidence: 99%

“…Digestion of Fg by plasmin in vivo is quite rare [19]. However, Fg degradation products generated during fibrinolysis are involved in tissue inflammation associated with various diseases [20,21].…”

Section: Introductionmentioning

confidence: 99%

Fibrinogen induces endothelial cell permeability

et al. 2007

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“…There is, however, evidence that cytokines, including TNF␣ and IL-1␤, act on perivascular cells to induce COX-2 activity, leading to production of PGE 2 that crosses the BBB and activates E-prostanoid receptors on central neurons to modulate cardiovascular control and sympathetic nerve activity (15,34). Indeed, intracarotid infusions of PGE 2 have been shown to increase arterial pressure and heart rate (4), and intracerebroventricular PGE 2 increased MAP, HR, and RSNA (35).…”

Section: Discussionmentioning

confidence: 99%

Role of prostaglandins in determining the increased cardiac sympathetic nerve activity in ovine sepsis

Booth

Ramchandra

Calzavacca

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Booth LC, Ramchandra R, Calzavacca P, May CN. Role of prostaglandins in determining the increased cardiac sympathetic nerve activity in ovine sepsis. Am J Physiol Regul Integr Comp Physiol 307: R75-R81, 2014. First published April 30, 2014 doi:10.1152/ajpregu.00450.2013.-Effective treatment of sepsis remains a significant challenge in intensive care units. During sepsis, there is widespread activation of the sympathetic nervous system, which is thought to have both beneficial and detrimental effects. The sympathoexcitation is thought to be partly due to the developing hypotension, but may also be a response to the inflammatory mediators released. Thus, we investigated whether intracarotid infusion of prostaglandin E2 (PGE2) induced similar cardiovascular changes to those caused by intravenous infusion of Escherichia coli in sheep and whether inhibition of prostaglandin synthesis, with the nonselective cyclooxygenase inhibitor indomethacin, administered at 2 and 8 h after the onset of sepsis, reduced sympathetic nerve activity (SNA), and heart rate (HR). Studies were performed in conscious sheep instrumented to measure mean arterial pressure (MAP), HR, cardiac SNA (CSNA), and renal SNA (RSNA). Intracarotid infusion of PGE2 (50 ng·kg Ϫ1 ·min Ϫ1 ) increased temperature, CSNA, and HR, but not MAP or RSNA. Sepsis, induced by infusion of E. coli, increased CSNA, but caused an initial, transient inhibition of RSNA. At 2 h of sepsis, indomethacin (1.25 mg/kg bolus) increased MAP and caused reflex decreases in HR and CSNA. After 8 h of sepsis, indomethacin did not alter MAP, but reduced CSNA and HR, without altering baroreflex control. These findings indicate an important role for prostaglandins in mediating the increase in CSNA and HR during the development of hyperdynamic sepsis, whereas prostaglandins do not have a major role in determining the early changes in RSNA.sepsis; cardiac sympathetic nerve activity; renal sympathetic nerve activity; PGE2; indomethacin; baroreflex curve; sheep SEPSIS AND SEPTIC SHOCK ARE the chief causes of death in intensive care units with mortality rates of between 30 and 70% when combined with multiorgan failure (2, 20, 21, 28). Although the incidence of sepsis is increasing, our knowledge of the pathology is limited, and current treatments, including volume resuscitation and vasoconstrictors, are only marginally effective. In human septic patients the most common hemodynamic profile is a hyperdynamic circulation, characterized by peripheral vasodilatation and hypotension accompanied by an increased cardiac output (16,17). These changes are accompanied by activation of the sympathetic nervous system, as demonstrated by increased circulating levels of plasma catecholamines in septic humans (12), increased renal sympathetic nerve activity (RSNA) in endotoxemic rats (22,30), and increased SNA to the heart and kidneys in sheep with hyperdynamic sepsis (24). It would be expected that an increase in SNA would be beneficial in sepsis, for example, by maintaining arterial pressure; however there...

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“…Earlier studies revealed that central infusion of pro-inflammatory cytokines such as IL-1β and TNF-α leads to significant hemodynamic and neurohormonal responses (such as increased arterial blood pressure) that are typical of CVDs, sympathetic activity, and the synthesis of renin, aldosterone and vasopressin [65,66] . Recent studies further showed that myocardial infarction induces the production of cytokines in the hypothalamus, which modulate neurotransmission in the PVN during the subsequent process of heart failure, resulting in elevated sympathoexcitation [67][68][69] .…”

Section: Brain Cytokines Act As Executors In the Association Between mentioning

confidence: 99%

Using optogenetics to translate the “inflammatory dialogue” between heart and brain in the context of stress

Cheng¹,

Zhang

et al. 2012

Neurosci. Bull.

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Abstract:Inflammatory processes are an integral part of the stress response and are likely to result from a programmed adaptation that is vital to the organism's survival and well-being. The whole inflammatory response is mediated by largely overlapping circuits in the limbic forebrain, hypothalamus and brainstem, but is also under the control of the neuroendocrine and autonomic nervous systems. Genetically predisposed individuals who fail to tune the respective contributions of the two systems in accordance with stressor modality and intensity after adverse experiences can be at risk for stress-related psychiatric disorders and cardiovascular diseases. Altered glucocorticoid (GC) homeostasis due to GC resistance leads to the failure of neural and negative feedback regulation of the hypothalamic-pituitary-adrenal axis during chronic inflammation, and this might be the mechanism underlying the ensuing brain and heart diseases and the high prevalence of co-morbidity between the two systems. By the combined use of light and genetically-encoded lightsensitive proteins, optogenetics allows cell-type-specific, fast (millisecond-scale) control of precisely defined events in biological systems. This method is an important breakthrough to explore the causality between neural activity patterns and behavioral profiles relevant to anxiety, depression, autism and schizophrenia. Optogenetics also helps to understand the "inflammatory dialogue", the inflammatory processes in psychiatric disorders and cardiovascular diseases, shared by heart and brain in the context of stress.

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

Cited by 45 publications

References 0 publications

Fibrinogen induces endothelial cell permeability

Fibrinogen induces endothelial cell permeability

Role of prostaglandins in determining the increased cardiac sympathetic nerve activity in ovine sepsis

Using optogenetics to translate the “inflammatory dialogue” between heart and brain in the context of stress

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