Abstract
Hypertension is the first modifiable vascular risk factor accounting for 10.4 million deaths worldwide; it is strongly and independently associated with the risk of stroke and is related to worse prognosis. In addition, hypertension seems to be a key player in the implementation of vascular cognitive impairment. Long-term hypertension, complicated or not by the occurrence of ischemic stroke, is often reviewed on its vascular side, and parenchymal consequences are put aside. Here, we sought to review the impact of isolated hypertension or hypertension associated to stroke on brain atrophy, neuron connectivity and neurogenesis, and phenotype modification of microglia and astrocytes. Finally, we discuss the impact of antihypertensive therapies on cell responses to hypertension and functional recovery. This attractive topic remains a focus of continued investigation and stresses the relevance of including this vascular risk factor in preclinical investigations of stroke outcome.
Highlights
Hypertension is the first modifiable risk factor, accounting for 10.4 million deaths and 218 million attributable disability-adjusted life-years worldwide [1]
Induced hypertension models are often used in preclinical research since they can be applied either to mice or rats. They consist of an oral or subcutaneous administration of pharmacoactive drugs involved in hypertension (namely angiotensin Angiotensin II (II) (Ag II), deoxycorticosterone acetate (DOCA), and N-nitro-L-arginine methyl ester (L-NAME)), with the duration of treatment depending on the severity of hypertension that is targeted
In Spontaneously hypertensive rats (SHR), in which cerebral ischemia was induced by the thermocoagulation of a distal branch of the middle cerebral artery, neutrophils, monocytes, and myeloid dendritic cells entered the brain at day 1, whereas microglial cell counts were comparable with the control condition, but increased by almost 300% at day 4 with a concomitant decrease of neutrophils and monocytes [99]
Summary
Hypertension is the first modifiable risk factor, accounting for 10.4 million deaths and 218 million attributable disability-adjusted life-years worldwide [1]. In a recent international study population that aimed to estimate hypertension prevalence, awareness, and medication control, only 46.5% of participants were aware that they suffered from hypertension, and only 32.5% of treated patients were pharmacologically controlled [4]. Increased blood pressure at the acute phase of stroke has been reported to increase the probability and severity of poststroke dementia [21], while the impact of chronic hypertension is still a matter of debate [22, 23]. After briefly addressing rodent hypertension and ischemic stroke (IS) models, we sought to review the impact of isolated hypertension or hypertension associated to IS on brain nonvascular cells and consequences on function. We discuss the impact of antihypertensive therapies on cell responses to hypertension and functional recovery
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