Rodent models demonstrate that chronic hypertension induces structural cerebrovascular alterations, blood-brain barrier disruption, microvascular rarefaction, and neuroinflammation.
Rodent models are essential for elucidating the pathophysiological mechanisms connecting chronic hypertension to brain damage, highlighting the potential therapeutic benefits of targeting the renin-angiotensin system.
Abstract Hypertension is a prevalent condition that significantly raises the incidence of cerebrovascular and cognitive disorders. This review focuses on the factors most closely linked to stroke, cognitive impairment, and Alzheimer’s disease. Research into pathophysiology and treatment of hypertensive brain damage has greatly benefited from rodent models, which have been crucial in uncovering the underlying mechanisms and developing effective therapeutic strategies. Rodent models, particularly spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHR-SP), have been essential in elucidating the pathophysiological mechanisms connecting hypertension to brain damage. These models exhibit structural and functional cerebrovascular alterations, including blood-brain barrier disruption, microvascular rarefaction, and neuroinflammation. Interventions targeting the renin-angiotensin system have shown promise in mitigating these adverse effects. This review synthesizes current findings from rodent studies, underscoring the pivotal impact of hypertension in brain pathology and the potential therapeutic benefits of antihypertensive treatments.
Scenna et al. (Tue,) conducted a review in Hypertension-associated brain damage. Rodent models demonstrate that chronic hypertension induces structural cerebrovascular alterations, blood-brain barrier disruption, microvascular rarefaction, and neuroinflammation.