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.