The effects of hypertension on the cerebral circulation

Abstract

Maintenance of brain function depends on a constant blood supply. Deficits in cerebral blood flow are linked to cognitive decline, and they have detrimental effects on the outcome of ischemia. Hypertension causes alterations in cerebral artery structure and function that can impair blood flow, particularly during an ischemic insult or during periods of low arterial pressure. This review will focus on the historical discoveries, novel developments, and knowledge gaps in 1) hypertensive cerebral artery remodeling, 2) vascular function with emphasis on myogenic reactivity and endothelium-dependent dilation, and 3) blood-brain barrier function. Hypertensive artery remodeling results in reduction in the lumen diameter and an increase in the wall-to-lumen ratio in most cerebral arteries; this is linked to reduced blood flow postischemia and increased ischemic damage. Many factors that are increased in hypertension stimulate remodeling; these include the renin-angiotensin-aldosterone system and reactive oxygen species levels. Endothelial function, vital for endothelium-mediated dilation and regulation of myogenic reactivity, is impaired in hypertension. This is a consequence of alterations in vasodilator mechanisms involving nitric oxide, epoxyeicosatrienoic acids, and ion channels, including calcium-activated potassium channels and transient receptor potential vanilloid channel 4. Hypertension causes blood-brain barrier breakdown by mechanisms involving inflammation, oxidative stress, and vasoactive circulating molecules. This exposes neurons to cytotoxic molecules, leading to neuronal loss, cognitive decline, and impaired recovery from ischemia. As the population ages and the incidence of hypertension, stroke, and dementia increases, it is imperative that we gain a better understanding of the control of cerebral artery function in health and disease.

Cerebral Hemodynamics in Normal Aging: Central Artery Stiffness, Wave Reflection, and Pressure Pulsatility

“…Individuals who are taking antihypertensive medications or participating in regular exercise were excluded for their potential impact on cerebral and central hemodynamics. [12][13][14] This study was approved by the Institutional Review Board of the University of Texas Southwestern Medical Center and Texas Health Presbyterian Hospital Dallas, and was performed in accordance with the guidelines of the Declaration of Helsinki and Belmont Report. All subjects gave informed written consent before participation.…”

The neuropathology and cerebrovascular mechanisms of dementia

“…83 Chronically elevated blood pressure promotes cerebrovascular remodeling, leading to a reduction in the lumen diameter by an increase in the wall-to-lumen ratio. 84 Additional consequences of prolonged systemic blood pressure include altered morphology of small cerebral arterioles that supply vulnerable brain regions necessary for cognitive function. 84 Epidemiologic and preclinical studies have recently begun to address the complex interactions between aging, hypertension, and AD pathology.…”

“…84 Additional consequences of prolonged systemic blood pressure include altered morphology of small cerebral arterioles that supply vulnerable brain regions necessary for cognitive function. 84 Epidemiologic and preclinical studies have recently begun to address the complex interactions between aging, hypertension, and AD pathology. The direct effects of hypertension on A accumulation have been shown in the brain parenchyma.…”

Hemorrhagic Transformation after Ischemic Stroke in Animals and Humans

“…52,139 Hypertension may also enhance formation of ROS, activation of MMPs, and inflammation and thus potentially promote BBB disruption and HT. 158 An interaction between age and hypertension may also exist. In a SHR stroke model, the rate of HT was the same in young rats compared with aged rats.…”