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Updated: Aug 27, 2025
Evaluation of Bioenergetic Function in Cerebral Vascular Endothelial Cells
Published on: November 19, 2016
Brain bioenergetics in chronic hypertension: Risk factor for acute ischemic stroke
Federica Ferrari1, Roberto Federico Villa2
1Department of Brain and Behavioural Sciences, School of Neurology - University of Pavia, Via Bassi 21, 27100 Pavia, Italy; Department of Biology and Biotechnology, University of Pavia, Via Ferrata 9, 27010 Pavia, Italy.
Insights
Chronic hypertension impairs brain energy metabolism and mitochondrial function, increasing stroke risk. Understanding these links is crucial for developing new treatments for hypertension and stroke.
Area of Science:
- Neuroscience
- Cardiovascular Science
- Mitochondrial Biology
Background:
- Chronic hypertension is a major risk factor for acute ischemic stroke.
- Hypertension alters brain bioenergetics, affecting cerebrovascular autoregulation and neuronal function.
- Existing adaptive mechanisms in hypertension are insufficient to maintain brain homeostasis.
Purpose of the Study:
- To review the mechanisms linking chronic hypertension, brain bioenergetics, and mitochondrial dysfunction to ischemic stroke risk.
- To explore the interplay between hemodynamic factors and metabolic processes in hypertension-related stroke.
- To consider the role of mitochondrial dysfunction in neurogenic hypertension and discuss future research directions.
Main Methods:
- Narrative review of experimental and clinical evidence.
- Discussion of mechanisms involving cerebral autoregulation, neurovascular coupling, and mitochondrial function.
- Analysis of the cause-effect relationships between hypertension and brain bioenergetic abnormalities.
Main Results:
- Alterations in brain bioenergetics and mitochondrial function in chronic hypertension increase stroke risk.
- Impaired cerebrovascular autoregulation and neurovascular coupling contribute to stroke pathogenesis.
- Mitochondrial dysfunction may play a role in the progression of chronic neurogenic hypertension.
Conclusions:
- Chronic hypertension-induced brain bioenergetic deficits and mitochondrial dysfunction are key contributors to ischemic stroke.
- Targeting brain bioenergetics and mitochondrial function may offer novel therapeutic strategies for hypertension and stroke.
- Further research is needed to elucidate the bidirectional relationship between chronic hypertension and brain bioenergetic abnormalities for translational applications.
Abstract:
Chronic hypertension is one of the key modifiable risk factors for acute ischemic stroke, also contributing to determine greater neurological deficits and worse functional outcome when an acute cerebrovascular event would occur. A tight relationship exists between cerebrovascular autoregulation, neuronal activity and brain bioenergetics. In chronic hypertension, progressive adaptations of these processes occur as an attempt to cope with the demanding necessity of brain functions, creating a new steady-state homeostatic condition. However, these adaptive modifications are insufficient to grant an adequate response to possible pathological perturbations of the established fragile hemodynamic and metabolic homeostasis. In this narrative review, we will discuss the main mechanisms by which alterations in brain bioenergetics and mitochondrial function in chronic hypertension could lead to increased risk of acute ischemic stroke, stressing the interconnections between hemodynamic factors (i.e. cerebral autoregulation and neurovascular coupling) and metabolic processes. Both experimental and clinical pieces of evidence will be discussed. Moreover, the potential role of mitochondrial dysfunction in determining, or at least sustaining, the pathogenesis and progression of chronic neurogenic hypertension will be considered. In the perspective of novel therapeutic strategies aiming at improving brain bioenergetics, we propose some determinant factors to consider in future studies focused on the cause-effect relationships between chronic hypertension and brain bioenergetic abnormalities (and vice versa), so to help translational research in this so-far unfilled gap.
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