Cerebral perfusion in untreated, controlled, and uncontrolled hypertension

Christie, Isabel N.; Windsor, Rowan; Mutsaerts, Henk‐Jan; Tillin, Therese; Sudre, Carole H.; Hughes, Alun D.; Golay, Xavier; Gourine, Alexander V.; Hosford, Patrick S.

doi:10.1177/0271678x221124644

Cited by 16 publications

(8 citation statements)

References 9 publications

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“…This is in line with previous rat studies that found angiogenic responses in chronic hypertension [69,78,87,88]. We previously showed that cortical blood flow is reduced in chronic hypertensive rats [11], similar to a recent large human MRI study that assessed cerebral blood flow [89].…”

Section: Angiogenesissupporting

confidence: 91%

Vascular and neural transcriptomics reveal stage-dependent pathways to inflammation and cognitive dysfunction in a rat model of hypertension

Ulbrich

Morton

Briese

et al. 2023

Preprint

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Chronic arterial hypertension causes cerebral microvascular dysfunction and doubles dementia risk in aging. However, cognitive health preservation by therapeutic blood pressure lowering alone is limited and depends on disease duration, the degree of irreversible tissue damage and whether microvascular function can be restored. This study aimed to understand molecular and cellular temporo-spatial pathomechanisms in the course of hypertension. We investigated the effects of initial, early chronic and late chronic hypertension in the frontal brain of rats by applying behavioral tests, histopathology, immunofluorescence, FACS, microvascular/neural tissue RNA sequencing as well as 18F-FDG PET imaging. Chronic hypertension caused frontal brain-specific behavioral deficits. Our results highlight stage-dependent responses to continuous microvascular stress and wounding by hypertension. Early responses included a fast recruitment of activated microglia to the blood vessels, immigration of peripheral immune cells, blood-brain-barrier leakage and an energy-demanding hypermetabolic state. Vascular adaptation mechanisms were observed in later stages and included angiogenesis and vessel wall strengthening by upregulation of cellular adhesion molecules and extracellular matrix. Additionally, we identified late chronic accumulation of Igfbp-5 in the brains of hypertensive rats, which is also a signature of Alzheimer dementia and attenuates protective Igf-1 signaling. Our study advances the knowledge of involved pathomechanisms and highlights the stage-dependent nature of hypertensive pathobiology. This groundwork might be helpful for basic and clinical research to identify stage-dependent markers in the human disease course, investigate stage-dependent interventions besides blood pressure lowering and better understand the relationship between poor vascular health and neurodegenerative diseases.

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Section: Angiogenesissupporting

confidence: 91%

Vascular and neural transcriptomics reveal stage-dependent pathways to inflammation and cognitive dysfunction in a rat model of hypertension

Ulbrich

Morton

Briese

et al. 2023

Preprint

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“…However, recent systematic review and meta-analyses suggest that potential effects of these medications on CBF in otherwise healthy older adults are likely to be minimal. [57][58][59]…”

Section: Strengths and Limitationsmentioning

confidence: 99%

Cerebral blood flow and cerebrovascular resistance across the adult lifespan: A multimodality approach

Tomoto

Khan

et al. 2023

J Cereb Blood Flow Metab

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Cerebral blood flow (CBF) decreases across the adult lifespan; however, more studies are needed to understand the underlying mechanisms. This study measured CBF and cerebrovascular resistance (CVR) using a multimodality approach in 185 healthy adults (21–80 years). Color-coded duplex ultrasonography and phase-contrast MRI were used to measure CBF, CBF velocity, and vessel diameters of the internal carotid (ICA) and vertebral arteries (VA). MRI arterial spin labeling was used to measure brain perfusion. Transcranial Doppler was used to measure CBF velocity at the middle cerebral artery. Structural MRI was used to measure brain volume. CBF was presented as total blood flow (mL/min) and normalized CBF (nCBF, mL/100g/min). Mean arterial pressure was measured to calculate CVR. Age was associated with decreased CBF by ∼3.5 mL/min/year and nCBF by ∼0.19 mL/100g/min/year across the methods. CVR increased by ∼0.011 mmHg/mL/100g/min/year. Blood flow velocities in ICA and VA decreased with age ranging from 0.07–0.15 cm/s/year, while the vessel diameters remained similar among age groups. These findings suggest that age-related decreases in CBF can be attributed mainly to decreases in blood flow velocity in the large cerebral arteries and that increased CVR likely reflects the presence of cerebral vasoconstrictions in the small cerebral arterioles and/or capillaries.

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“…181,183,214 Under normal conditions, CBF gradually declines with increasing age in both men and women. 189,215 This decline can be accelerated in the presence of hypertension 26,[216][217][218] or conditions such as heart failure. 160 Based primarily on temporal relationships, many studies have suggested that reductions in CBF begin before the onset of cognitive decline but are accelerated in the presence of hypertension (Figure 1).…”

Section: Cerebral Blood Flowmentioning

confidence: 99%

“…160 Based primarily on temporal relationships, many studies have suggested that reductions in CBF begin before the onset of cognitive decline but are accelerated in the presence of hypertension (Figure 1). 160,216,218,219 For example, in a population-based study with an almost 7-year follow-up, there was an association between reductions in CBF and subsequent cognitive deficits. 220 Lower CBF at baseline was associated with an increased rate of cognitive decline, particularly for memory and executive function, and a higher risk of dementia.…”

Section: Cerebral Blood Flowmentioning

confidence: 99%

Hypertension: Causes and Consequences of Circadian Rhythms in Blood Pressure

Faraci,

Scheer

2024

Circulation Research

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Hypertension is extremely common, affecting approximately 1 in every 2 adults globally. Chronic hypertension is the leading modifiable risk factor for cardiovascular disease and premature mortality worldwide. Despite considerable efforts to define mechanisms that underlie hypertension, a potentially major component of the disease, the role of circadian biology has been relatively overlooked in both preclinical models and humans. Although the presence of daily and circadian patterns has been observed from the level of the genome to the whole organism, the functional and structural impact of biological rhythms, including mechanisms such as circadian misalignment, remains relatively poorly defined. Here, we review the impact of daily rhythms and circadian systems in regulating blood pressure and the onset, progression, and consequences of hypertension. There is an emphasis on the impact of circadian biology in relation to vascular disease and end-organ effects that, individually or in combination, contribute to complex phenotypes such as cognitive decline and the loss of cardiac and brain health. Despite effective treatment options for some individuals, control of blood pressure remains inadequate in a substantial portion of the hypertensive population. Greater insight into circadian biology may form a foundation for novel and more widely effective molecular therapies or interventions to help in the prevention, treatment, and management of hypertension and its related pathophysiology.

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Cerebral perfusion in untreated, controlled, and uncontrolled hypertension

Cited by 16 publications

References 9 publications

Vascular and neural transcriptomics reveal stage-dependent pathways to inflammation and cognitive dysfunction in a rat model of hypertension

Vascular and neural transcriptomics reveal stage-dependent pathways to inflammation and cognitive dysfunction in a rat model of hypertension

Cerebral blood flow and cerebrovascular resistance across the adult lifespan: A multimodality approach

Hypertension: Causes and Consequences of Circadian Rhythms in Blood Pressure

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