Abstract
Background: The aorta plays a crucial role in the blood circulation through its Windkessel function, buffering blood volume and regulating blood pressure. While traditionally viewed as primarily passive, this function may be actively regulated by vascular smooth muscle cells in the aortic wall through vasoconstriction or -dilation. Despite the widespread use of antihypertensive drugs that target vascular tone, our understanding of human aortic vasoreactivity remains limited. This review therefore aimed to evaluate the vasoreactivity of the human aorta in response to various pharmacological and non-pharmacological stimuli. Summary: A systematic search of the PubMed database was conducted for articles published before January 1, 2024. Of the 1,179 articles that were screened for inclusion, 30 articles met the inclusion criteria. Ten studies involved ex vivo examinations, while 20 studies involved in vivo measurements. Ex vivo pharmacological testing revealed vasoconstriction induced by adrenergic and endothelin-A receptor agonists and prostanoids. Pharmacological vasodilation was observed following in vivo or ex vivo administration of nitrates and calcium channel blockers, although acetylcholine did not induce vasodilation ex vivo. Additionally, tobacco smoking and intravenous cocaine use were associated with vasoconstriction, whereas anesthetic agents were involved in potential aortic vasodilation. Key Messages: These findings challenge the traditional view of the aorta as a passive conduit, highlighting its vasoconstrictive and vasodilative properties in response to vasoactive stimuli. This revised understanding has significant implications for prescribing antihypertensive drugs, which commonly have vasodilatory effects. The potential impact of these vasoactive therapies on the aorta's Windkessel function warrants careful consideration, particularly in patients with aortic pathologies.The human body's largest blood vessel, the aorta, does more than just carry blood from the heart. It acts like a shock absorber, helping smooth out the pulsing blood flow and maintain steady circulation throughout the body. Traditionally, this pressure regulating system is viewed as purely a result of the aorta's elastic properties - essentially acting like a passive rubber tube. However, emerging research suggests that the muscle cells in the aorta wall can tighten or relax and can thereby actively change the aorta's elastic properties. This study examined previous literature to better understand how the human aorta responds to different substances and conditions. The analysis revealed that the aorta can actively change its diameter in response to various stimuli. Specific drugs and chemical pathways were identified that can cause the aorta to either contract or expand. For example, some common blood pressure medications were shown to expand the aortic wall. The findings of this study challenge the traditional view of the aorta as simply a passive tube: instead, the aorta is an active determinant of blood pressure. When treating high blood pressure, understanding how blood pressure medications affect the aorta's shock-absorbing function could influence how doctors prescribe such medications - especially in patients with aortic diseases.
| Original language | English |
|---|---|
| Pages (from-to) | 121-139 |
| Number of pages | 19 |
| Journal | Pulse (Basel, Switzerland) |
| Volume | 13 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2025 |
Bibliographical note
Copyright the Author(s) 2025. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.Keywords
- Aorta
- Human
- Vasoconstriction
- Vasodilation
- Vasoreactivity
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