Centrally administered interleukin-1 beta sensitizes to the central pressor action of angiotensin II

Ufnal, Marcin; Dudek, Magdalena; Żera, Tymoteusz; Szczepañska‐Sadowska, Ewa

doi:10.1016/j.brainres.2006.04.122

Cited by 21 publications

(18 citation statements)

References 28 publications

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“…14,15 It is rather unlikely that the dose of losartan was too small to block the brain AT1 receptors as it was sufficient to inhibit the pressor response to 20 ng of centrally infused Ang II in the simvastatin group. In addition, the same dose of ICV-infused losartan effectively abolished the pressor effect of centrally applied Ang II in our previous experiments 9 and in the studies of other authors. 15 These results suggest that under resting conditions inhibition of the brain angiotensinergic transmission may have no effect on hemodynamic parameters, likely due to the compensatory changes in activity of other blood pressure regulating systems, such as vasopressin system.…”

Section: Discussionmentioning

confidence: 81%

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Simvastatin Reduces Pressor Response to Centrally Administered Angiotensin II

Ufnal

Sikora

Żera

et al. 2010

American Journal of Hypertension

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Section: Discussionmentioning

confidence: 81%

“…The detailed methodology has been described elsewhere. 9 Compounds. The following drugs were used: commercially available simvastatin (Simratio 20 mg tablets; Ratiopharm, Warsaw, Poland), AT1 receptor antagonist (losartan; SigmaAldrich, Poznan, Poland), and Ang II (Sigma-Aldrich).…”

Section: Resultsmentioning

confidence: 99%

Simvastatin Reduces Pressor Response to Centrally Administered Angiotensin II

Ufnal

Sikora

Żera

et al. 2010

American Journal of Hypertension

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“…over a 2-min period at 1-week intervals before either continuing on control diet or switching to 5 days of ethanol-containing liquid diet (Figure 1). This 100-ng dose of the cytokines was initially chosen from literature as one having consistent effects on other functions (Ufnal et al, 2006;Plata-Salaman and Borkoski, 1994;Plata-Salaman et al, 1996). After showing that the 100-ng dose of TNFa sensitized withdrawal-induced anxiety, several doses of TNFa were chosen to determine if lower doses would have a similar consequence.…”

Section: Repeated Exposure To Lps and Selected Cytokines Before Chronmentioning

confidence: 99%

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Breese

Knapp

Overstreet

et al. 2007

Neuropsychopharmacol

100

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Previous investigations demonstrated that repeated stresses before an ethanol exposure sensitize ethanol withdrawal-induced anxietylike behavior ('anxiety'). In addition to activating the hypothalamic-pituitary-adrenal axis, acute stress also elevates cytokines in brain. Initially, to test possible cytokine involvement in this stress/withdrawal protocol, cytokines were increased in brain with 2 weekly repeated lipopolysaccharide (LPS) administrations (1000 m/kg) (LPS/withdrawal protocol) or with twice weekly intracerebroventricular (i.c.v.) administrations of the cytokines IL-1b, CCL2 (MCP-1) or TNFa (cytokine/withdrawal protocol) before exposure and withdrawal from a 5-day cycle of chronic ethanol diet. Both protocols sensitized withdrawal-induced anxiety and confirm cytokine involvement in the sensitized anxiety response. Testing of various doses of LPS (16-1000 mg/kg) and TNFa (3-100 ng, i.c.v.) demonstrated the dose-related nature of these protocols to sensitize withdrawal-induced anxiety. The sensitized anxiety was not produced by a single 5-day ethanol diet cycle or by repeated LPS or cytokine treatments alone. Likewise, sensitized anxiety in these protocols could not be attributed to differences in ethanol ingestion. When challenged with a subsequent re-exposure to a 5-day ethanol diet cycle 16 days after completion of the LPS/withdrawal or cytokine/withdrawal protocols, an increase in withdrawal-induced anxiety was observedFan indication of induction of an underlying persistent adaptive change. Finally, just as found previously with the stress/withdrawal protocol, administration of the benzodiazepine receptor antagonist flumazenil before the LPS or TNF treatments prevented anxiety sensitization. Together, these findings indicate that increased cytokine activity induces adaptive change that supports sensitization of ethanol withdrawal-induced anxiety that may be linked to GABA A -receptor function.

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“…[20, 21] Ang II raises BP via its peripheral and central effects. In the brain, ANG II downregulates neuronal NOS (nNOS) and leads to the decrease of NO production and the increase of SNS activity [8, 9, 18, 24]. There are also observations that IL-1 β downregulates SNS activity by increased local expression of NOS mRNA as well as that Ang II-mediated increases in arterial BP can be caused by inhibition of the expression of IL-1 β and nNOS at the brain level [10].…”

Section: Discussionmentioning

confidence: 99%

Proinflammation and Hypertension: A Population-Based Study

Vanhala

Kautiainen²,

Kumpusalo

2008

Mediators of Inflammation

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There is evidence that proinflammation may be linked to the development of hypertension (HT). We examined the association of both the interleukin-1 beta (IL-1β) and the interleukin 1-receptor antagonist (IL-1ra) with future blood pressure (BP) and HT occurrence (BP ≥ 140/90 mmHg, or antihypertensive drug) in a population-based prospective study. Our study consisted of 396 (147 men and 249 women) middle-aged, baseline apparently healthy, normotensive subjects participating in a 6.5-year follow-up study. Subjects with high-sensitivity CRP (hs-CRP) < 10 mg/L were excluded at the initial visit. At follow-up, the occurrence of HT was 32%. The levels of baseline IL-1β and IL-1ra were significantly higher for subjects who developed HT during the follow-up than for those who did not (IL-1β; 0.67 ± 0.62 pg/mL versus 0.56 ± 0.32 pg/mL, P = .020 and IL-1ra; 184 ± 132 pg/mL versus 154 ± 89 pg/mL, P = .007). After adjustments for age, follow-up time, sex, baseline systolic BP, and BMI, our results confirm a statistically significant (P = .036) linear association between the quartiles of IL-1β and change of systolic BP during the study. After adjustments for age, follow-up time, sex, and BMI, our results also show a linear association between incident HT and the quartiles of IL-1ra. (P = .026). These results provide evidence that proinflammation may precede BP elevation and HT.

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Centrally administered interleukin-1 beta sensitizes to the central pressor action of angiotensin II

Cited by 21 publications

References 28 publications

Simvastatin Reduces Pressor Response to Centrally Administered Angiotensin II

Simvastatin Reduces Pressor Response to Centrally Administered Angiotensin II

Repeated Lipopolysaccharide (LPS) or Cytokine Treatments Sensitize Ethanol Withdrawal-Induced Anxiety-Like Behavior

Proinflammation and Hypertension: A Population-Based Study

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