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Microcirculation and hypertension: The cause and the victim

Par : Type de matériel : TexteTexteLangue : français Détails de publication : 2025. Ressources en ligne : Abrégé : Microcirculation is made up of arterioles, capillaries, and venules with a diameter of less than 20 μm; it plays a fundamental role in oxygen supply, nutrient exchange, and maintenance of tissue homeostasis. Hypertension and microcirculation form a vicious circle: Changes in microcirculation precede and contribute to the pathophysiology of hypertension. Hypertension, in turn, provokes and aggravates both structural and functional alterations in microcirculation, which contribute to systemic and target-organ-specific vascular damage. In hypertension, microvascular remodeling and rarefaction lead to a reduction in microvascular density, which in turn contributes to increased vascular resistance and insufficient perfusion of target organs (heart, brain, kidneys, retina). The pathophysiological mechanisms underlying microvascular dysfunction in hypertension include endothelial dysfunction and oxidative stress. These changes reduce the bioavailability of nitric oxide (NO), increase the production of reactive oxygen species (ROS), and promote inflammation and fibrosis of vascular walls and surrounding tissues. This review highlights the central role of microvascular dysfunction in hypertension-related complications and underscores the importance of early detection and therapeutic interventions. Strategies to optimize blood pressure control, improve endothelial function, and target oxidative stress and vascular remodeling are essential to mitigate the systemic consequences of hypertension-related microvascular damage and to reduce the burden of the resulting cardiovascular and renal diseases.
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Microcirculation is made up of arterioles, capillaries, and venules with a diameter of less than 20 μm; it plays a fundamental role in oxygen supply, nutrient exchange, and maintenance of tissue homeostasis. Hypertension and microcirculation form a vicious circle: Changes in microcirculation precede and contribute to the pathophysiology of hypertension. Hypertension, in turn, provokes and aggravates both structural and functional alterations in microcirculation, which contribute to systemic and target-organ-specific vascular damage. In hypertension, microvascular remodeling and rarefaction lead to a reduction in microvascular density, which in turn contributes to increased vascular resistance and insufficient perfusion of target organs (heart, brain, kidneys, retina). The pathophysiological mechanisms underlying microvascular dysfunction in hypertension include endothelial dysfunction and oxidative stress. These changes reduce the bioavailability of nitric oxide (NO), increase the production of reactive oxygen species (ROS), and promote inflammation and fibrosis of vascular walls and surrounding tissues. This review highlights the central role of microvascular dysfunction in hypertension-related complications and underscores the importance of early detection and therapeutic interventions. Strategies to optimize blood pressure control, improve endothelial function, and target oxidative stress and vascular remodeling are essential to mitigate the systemic consequences of hypertension-related microvascular damage and to reduce the burden of the resulting cardiovascular and renal diseases.

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