Vascular and parenchymal lesions along with enhanced neurogenesis characterize the brain of asymptomatic stroke-prone spontaneous hypertensive rats

Cova, Lidia; Mura, E La; Mauro, Alessandro; Stramba-Badiale, Marco; Michailidis, Georgios; Colonna, A.; Assawy, Nadia El; Pignieri, Alice; Busca, Giuseppe; Tremoli, Elena; Silani, Vincenzo; Sironi, Luigi; Zanchetti, Alberto

doi:10.1097/hjh.0b013e3283619d7f

Cited by 5 publications

(6 citation statements)

References 46 publications

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“…The mechanisms that connect alimentary sodium to stroke have been discussed in recent years and range from vascular lesions with enhanced neurogenesis [110], to endothelial dysfunction [111], inflammation due to low parasympathetic activity [112], small vessel disease associated with high sodium consumption [113], adenosine receptor expression [114] or other protein expression, and microglia polarization [115].…”

Section: Sodium Intake and Cardiovascular Eventsmentioning

confidence: 99%

Sodium Intake and Target Organ Damage in Hypertension—An Update about the Role of a Real Villain

Nista

Gatto

Albertelli

et al. 2020

IJERPH

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Salt intake is too high for safety nowadays. The main active ion in salt is sodium. The vast majority of scientific evidence points out the importance of sodium restriction for decreasing cardiovascular risk. International Guidelines recommend a large reduction in sodium consumption to help reduce blood pressure, organ damage, and cardiovascular risk. Regulatory authorities across the globe suggest a general restriction of sodium intake to prevent cardiovascular diseases. In spite of this seemingly unanimous consensus, some researchers claim to have evidence of the unhealthy effects of a reduction of sodium intake, and have data to support their claims. Evidence is against dissenting scientists, because prospective, observational, and basic research studies indicate that sodium is the real villain: actual sodium consumption around the globe is far higher than the safe range. Sodium intake is directly related to increased blood pressure, and independently to the enlargement of cardiac mass, with a possible independent role in inducing left ventricular hypertrophy. This may represent the basis of myocardial ischemia, congestive heart failure, and cardiac mortality. Although debated, a high sodium intake may induce initial renal damage and progression in both hypertensive and normotensive subjects. Conversely, there is general agreement about the adverse role of sodium in cerebrovascular disease. These factors point to the possible main role of sodium intake in target organ damage and cardiovascular events including mortality. This review will endeavor to outline the existing evidence.

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Section: Sodium Intake and Cardiovascular Eventsmentioning

confidence: 99%

Sodium Intake and Target Organ Damage in Hypertension—An Update about the Role of a Real Villain

Nista

Gatto

Albertelli

et al. 2020

IJERPH

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“…With the worsening of the proteinuria to over 100mg/day changes are seen in the brain in the subventricular zone with higher levels of nestin, GFAP, and doublecortin, indicating the emergence of immature neural stem cells and that only new astrocytes can survive. At this stage, no MRI-detectable lesions are seen (Cova et al, 2013). …”

Section: Introductionmentioning

confidence: 98%

Rodent Models of Vascular Cognitive Impairment

Yang

Kimura-Ohba

Thompson

et al. 2016

Transl. Stroke Res.

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Vascular cognitive impairment dementia (VCID), which is an increasingly important cause of dementia in the elderly, lacks effective treatments. Many different types of vascular disease are included under the diagnosis of VCID, including large vessel disease with multiple strokes, and small vessel disease with lacunar infarcts and white matter disease. Animal models have been developed to study the multiple forms of VCID. Because of its progressive course, small vessel disease (SVD) is thought to be the optimal form of VCID for treatment. One theory is that the pathophysiology involves hypoxic hypoperfusion resulting in injury to the white matter and neuronal death. Bilateral occlusion of the common carotid arteries (BCAO) in a normotensive rat, which reduces cerebral blood flow, induces hypoxia with white matter damage; this model has been used to test drugs to block the injury. Another model is the spontaneously hypertensive/stroke prone rat (SHR/SP). Hypertension leads to small vessel disease resulting in progressive damage to the white matter, cortex and hippocampus. Bilateral carotid artery stenosis (BCAS) with coils or ameroid constrictors produces a slower development of changes than BCAO, avoiding the acute ischemia. A few studies have been done with the two-clip, two-vessel occlusion renal model for induction of hypertension. There are benefits and drawbacks to each of these models with the model selected depending on the type of vascular damage that is to be studied. This review describes the most commonly used models, and the drugs that have been used to reduce the damage.

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Section: Role Of Brain Pericytes In Neurological Disorders Associated...mentioning

confidence: 97%

“…In a genetic model of severe hypertension and increased occurrence of stroke, rats exhibit low levels of proteinuria (implying kidney disease) that appear at the time of initial cerebrovascular injury (Cova et al 2013). Consistent with a role for pericyte damage in causing the cerebral injury, the injury includes cerebral vasogenic oedema, lacunar infarcts and focal cell loss (Cova et al 2013), which have all been associated with pericyte dysfunction in other diseases, such as stroke, amyotrophic lateral sclerosis and Alzheimer's disease (Yemisci et al 2009;Sengillo et al 2013;Winkler et al 2013).…”

Section: Kidney-brain Signallingmentioning

confidence: 98%

The role of pericytes in brain disorders: from the periphery to the brain

Hirunpattarasilp

Attwell

Freitas

2019

Journal of Neurochemistry

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It is becoming increasingly apparent that disorders of the brain microvasculature contribute to many neurological disorders. In recent years it has become clear that a major player in these events is the capillary pericyte which, in the brain, is now known to control the blood–brain barrier, regulate blood flow, influence immune cell entry and be crucial for angiogenesis. In this review we consider the under‐explored possibility that peripheral diseases which affect the microvasculature, such as hypertension, kidney disease and diabetes, produce central nervous system (CNS) dysfunction by mechanisms affecting capillary pericytes within the CNS. We highlight how cellular messengers produced peripherally can act via signalling pathways within CNS pericytes to reshape blood vessels, restrict blood flow or compromise blood–brain barrier function, thus causing neuronal dysfunction. Increased understanding of how renin–angiotensin, Rho‐kinase and PDGFRβ signalling affect CNS pericytes may suggest novel therapeutic approaches to reducing the CNS effects of peripheral disorders.

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Vascular and parenchymal lesions along with enhanced neurogenesis characterize the brain of asymptomatic stroke-prone spontaneous hypertensive rats

Abstract: Appearance of vascular changes in SHRSPs, before any MRI-detectable brain lesion, is coupled to active neural proliferation in the SVZ. With disease progression, only newborn astrocytes can survive, likely because of the neurotoxicity triggered by brain oedema and oxidative stress.

Cited by 5 publications

References 46 publications

Sodium Intake and Target Organ Damage in Hypertension—An Update about the Role of a Real Villain

Sodium Intake and Target Organ Damage in Hypertension—An Update about the Role of a Real Villain

Rodent Models of Vascular Cognitive Impairment

The role of pericytes in brain disorders: from the periphery to the brain

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