Cerebrovascular Function in Pregnancy and Eclampsia

Department of Neurology, University of Vermont College of Medicine, Burlington, VT 05405, USA.
Hypertension (Impact Factor: 6.48). 08/2007; 50(1):14-24. DOI: 10.1161/HYPERTENSIONAHA.106.079442
Source: PubMed

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    • "One study shows that 16% of cases of eclampsia occur in normotensive patients, and only 13% of cases were associated with severe hypertension [68, 69]. Therefore, the loss of autoregulation of cerebral perfusion secondary to hypertension does not explain all cases of PRES, so that alteration of endothelial permeability by disruption of the BBB ought to play an important role [67]. A recent study shows that preeclampsia altered BBB permeability independently of blood pressure. "
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    ABSTRACT: Preeclampsia is a common disease of pregnancy characterized by the presence of hypertension and commitment of many organs, including the brain, secondary to generalized endothelial dysfunction. Its etiology is not known precisely, but it involved several factors, highlighting the renin angiotensin system (RAS), which would have an important role in the origin of multisystem involvement. This paper reviews the evidence supporting the involvement of RAS in triggering the disease, in addition to the components of this system that would be involved and how it eventually produces brain engagement.
    Full-text · Article · Dec 2012 · International Journal of Hypertension
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    • "Cerebral blood vessels are the premier target of the brain damage produced by hypertension, a major risk factor for stroke and dementia (Iadecola and Davisson, 2008; Unverzagt et al., 2011). Chronic hypertension is well known to alter cerebrovascular structure and function (Cipolla, 2007). In particular, hypertension disrupts vital neurovascular mechanisms coupling the local delivery of blood flow with the energetic needs of active brain regions (Kazama et al., 2004; Jennings et al., 2005; Iadecola and Davisson, 2008). "
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    ABSTRACT: Hypertension, a powerful risk factor for stroke and dementia, has damaging effects on the brain and its vessels. In particular, hypertension alters vital cerebrovascular control mechanisms linking neural activity to cerebral perfusion. In experimental models of slow-developing hypertension, free radical signaling in the subfornical organ (SFO), one of the forebrain circumventricular organs, is critical for the hormonal release and sympathetic activation driving the elevation in arterial pressure. However, the contribution of this central mechanism to the cerebrovascular alterations induced by hypertension remains uncertain. We tested the hypothesis that free radical production in the SFO is involved in the alterations in cerebrovascular regulation produced by hypertension. In a mouse model of gradual hypertension induced by chronic administration of subpressor doses of angiotensin II (AngII), suppression of free radicals in the SFO by overexpression of CuZn-superoxide dismutase (CuZnSOD) prevented the alteration in neurovascular coupling and endothelium-dependent responses in somatosensory cortex induced by hypertension. The SFO mediates the dysfunction via two signaling pathways. One involves SFO-dependent activation of the paraventricular hypothalamic nucleus, elevations in plasma vasopressin, upregulation of endothelin-1 in cerebral resistance arterioles and activation of endothelin type A receptors. The other pathway depends on activation of cerebrovascular AngII type 1 (AT1) receptors by AngII. Both pathways mediate vasomotor dysfunction by inducing vascular oxidative stress. The findings implicate for the first time the SFO and its efferent hypothalamic pathways in the cerebrovascular alterations induced by AngII, and identify vasopressin and endothelin-1 as potential therapeutic targets to counteract the devastating effects of hypertension on the brain.
    Full-text · Article · Apr 2012 · The Journal of Neuroscience : The Official Journal of the Society for Neuroscience
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    • "Hypertension has detrimental effects on cerebral blood flow in humans (Lipsitz et al., 2005; Beason-Held et al., 2007; Dai et al., 2008; Efimova et al., 2008; Nagata et al., 2010; Waldstein et al., 2010; Muller et al., 2012). Hypertension is associated with a shift in the autoregulatory curve to the right (Cipolla, 2007; Iadecola and Davisson, 2008). This means that during hypertension, higher pressures are needed to maintain cerebral perfusion in the normal range. "
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    ABSTRACT: Oxidative stress has emerged as a key component of many diseases that affect the vasculature. Oxidative stress is characterized as a cellular environment where the generation of oxidant molecules overwhelms endogenous anti-oxidant defense mechanisms. NADPH oxidases are a family of enzymes whose primary purpose is generation of reactive oxygen species (oxidant molecules) and therefore are likely to be key contributors to oxidative stress. Hypertension is associated with oxidative stress in the vasculature and is a major risk factor for stroke and cognitive abnormalities. Angiotensin II (Ang II) is the main effector peptide of the renin-angiotensin system (RAS) and plays a critical role in promoting oxidative stress in the vasculature. In the cerebral circulation, Ang II has been implicated in reactive oxygen species generation, alterations to vasomotor function, impaired neurovascular coupling, inflammation, and vascular remodeling. Furthermore, studies in humans have shown that cerebral blood flow is altered during hypertension and therapeutically targeting the RAS improves cerebral blood flow. Importantly, many of the aforementioned effects have been shown to be dependent on NADPH oxidases. Thus, Ang II, NADPH oxidases and oxidative stress are likely to play key roles in the pathogenesis of hypertension and associated cerebrovascular disease. This review will focus on our current understanding of the contribution of Ang II and NADPH oxidases to oxidative stress in the cerebral circulation.
    Full-text · Article · Jan 2012 · Frontiers in Physiology
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