Microcirculation and hypertension: The cause and the victim (notice n° 1528986)

détails MARC
000 -LEADER
fixed length control field 02130cam a2200157 4500500
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20251012013252.0
041 ## - LANGUAGE CODE
Language code of text/sound track or separate title fre
042 ## - AUTHENTICATION CODE
Authentication code dc
100 10 - MAIN ENTRY--PERSONAL NAME
Personal name Lévy, Bernard
Relator term author
245 00 - TITLE STATEMENT
Title Microcirculation and hypertension: The cause and the victim
260 ## - PUBLICATION, DISTRIBUTION, ETC.
Date of publication, distribution, etc. 2025.<br/>
500 ## - GENERAL NOTE
General note 48
520 ## - SUMMARY, ETC.
Summary, etc. 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.
786 0# - DATA SOURCE ENTRY
Note Sang Thrombose Vaisseaux | Volume 37 | 1 | 2025-03-28 | p. 16-26 | 0999-7385
856 41 - ELECTRONIC LOCATION AND ACCESS
Uniform Resource Identifier <a href="https://shs.cairn.info/journal-sang-thrombose-vaisseaux-2025-1-page-16?lang=en&redirect-ssocas=7080">https://shs.cairn.info/journal-sang-thrombose-vaisseaux-2025-1-page-16?lang=en&redirect-ssocas=7080</a>

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