Brain nuclear factor-kappa B activation contributes to neurohumoral excitation in angiotensin II-induced hypertension

Abstract

These findings suggest that an ANG II-induced increase in the brain renin-angiotensin system activates NF-kappaB in the PVN and contributes to sympathoexcitation in hypertension. The increased superoxide in the PVN contributes to NF-kappaB activation and neurohumoral excitation in hypertension.

Prenatal exposure to lipopolysaccharide alters the intrarenal renin–angiotensin system and renal damage in offspring rats

“…Ang II infusion results in a significant upregulation of NF-kB, RAS, proinflammatory cytokines and oxidative stress, and the interplay between RAS, proinflammatory cytokines and NF-kB leads to a sustained increase in oxidative stress, which contributes to the pathogenesis of hypertension. 2 It was found in this study that the most effective inhibitor of Figure 4 Electrophoretic mobility shift assay (EMSA) for the nuclear transcription factor (NF)-kB in kidney of rats at 25 weeks of age. Nuclear protein was extracted from the kidneys of 25-week-old rats.…”

“…1 A growing body of evidence indicates that hypertension is an inflammatory state wherein proinflammatory cytokines, such as tumor necrosis factor-a and interleukin-6, contribute to the hypertensive effect. [2][3][4][5] Angiotensin II (Ang II), the major biologically active component of the reninangiotensin system (RAS), not only induces vasoconstriction, aldosterone release and sodium reabsorption by the nephron, but is also intricately interrelated with inflammation. Furthermore, the association of Ang II and inflammation induces an amplification process that involves oxidative stress and proinflammatory transcription factors, leading to progressive vascular injury 6 and having an important role in the development of hypertension and target organ damage.…”

“…Furthermore, the association of Ang II and inflammation induces an amplification process that involves oxidative stress and proinflammatory transcription factors, leading to progressive vascular injury 6 and having an important role in the development of hypertension and target organ damage. 2 It has been shown in our laboratory that maternal exposure to lipopolysaccharide (LPS) results in hypertension in offspring rats. 7 However, the mechanisms are not well understood.…”

TNF-.ALPHA. in Hypothalamic Paraventricular Nucleus Contributes to Sympathoexcitation in Heart Failure by Modulating AT1 Receptor and Neurotransmitters

“…Recent studies also suggest that proinflammatory cytokines and the renin-angiotensin system (RAS) can contribute to these changes (Kang et al 2008a(Kang et al , 2008b(Kang et al , 2009a(Kang et al , 2009b. Our laboratory and others have reported that cytokine blockade in the brain decreases components of the RAS (Kang et al 2008b, Guggilam et al 2008 and that RAS blockade attenuates production of proinflammatory cytokines (Kang et al 2008a(Kang et al , 2009b.…”

“…Recent studies also suggest that proinflammatory cytokines and the renin-angiotensin system (RAS) can contribute to these changes (Kang et al 2008a(Kang et al , 2008b(Kang et al , 2009a(Kang et al , 2009b. Our laboratory and others have reported that cytokine blockade in the brain decreases components of the RAS (Kang et al 2008b, Guggilam et al 2008 and that RAS blockade attenuates production of proinflammatory cytokines (Kang et al 2008a(Kang et al , 2009b. We inhibited cytokine synthesis in the brain with centrally infused pentoxifylline (PTX) and found that lowering hypothalamic levels of TNF-α and IL-1β without changing plasma cytokine levels is associated with reductions in brain renin, ACE, and AT1-R, strongly suggests that proinflammatory cytokines are intrinsically involved in regulating brain RAS, and thus sympathetic nerve activity and extracellular fluid volume, in rats with HF.…”