Time‐of‐day variation in vascular function
Open accessAbstract
New Findings: What is the topic of this review? This report looks at the role of endothelial nitric oxide signalling in the time‐of‐day variation in vasoconstriction of resistance vessels. What advances does it highlight? It highlights a time‐of‐day variation in contraction of mesenteric arteries, characterized by a reduced contractile response to either phenylephrine or high K+ and increased relaxation in response to acetylcholine during the active period. This time‐of‐day variation in contraction results from a difference in endothelial nitric oxide synthase (eNOS) signalling that correlates with levels of eNOS expression, which peak during the active period and may have far reaching physiological consequences beyond regulation of blood pressure. There is a strong time‐of‐day variation in the vasoconstriction in response to sympathetic stimulation that may contribute to the time‐of‐day variation in blood pressure, which is characterized by a dip in blood pressure during the individual's rest period when sympathetic activity is low. Vasoconstriction is known to be regulated tightly by nitric oxide signalling from the endothelial cells, so we have looked at the effect of time‐of‐day on levels of endothelial nitric oxide synthase (eNOS) and vascular contractility. Mesenteric arteries isolated from the nocturnal rat exhibit a time‐of‐day variation in their contractile response to α 1‐adrenoreceptor and muscarinic activation, which is characterized by a reduced vasoconstriction in response to phenylephrine and enhanced vasodilatation in response to acetylcholine during the rat's active period at night. An increase in eNOS signalling during the active period is responsible for this time‐of‐day difference in response to phenylephrine and acetylcholine and correlates with the large increase in eNOS expression (mRNA and protein) during the active period, possibly driven by the presence of a functioning peripheral circadian clock. This increase in eNOS signalling may function to limit the increase in peripheral resistance and therefore blood pressure during the increased sympathetic activity.
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Candidate mechanisms for elevated cardiovascular disease risk due to shift work include disrupted 24-hour rhythms of blood pressure and vascular function, atherosclerosis, proinflammatory states, and altered lipid and glucose metabolism.
“Candidate mechanisms underlying elevated risk for CVD due to shift work include disrupted 24-hour rhythms of blood pressure [84] and vascular function [85], atherosclerosis [86], proinflammatory states [87], and altered lipid and glucose metabolism [88].”
From Shift Work: Disrupted Circadian Rhythms and Sleep—Implications for Health and Well-being (2017) · cites this paper as [85]
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Shift Work: Disrupted Circadian Rhythms and Sleep—Implications for Health and Well-being
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- Authors
- Rodrigo, G. C., & Denniff, M.
- Affiliations
- University of Leicester (GB)
- Corresponding author
- Rodrigo, G. C.
- Venue
- Experimental Physiology
- Publisher
- Wiley
- Published
- 2016-07-30
- Volume
- 101
- Issue
- 8
- Pages
- 1030-1034
- ISSN
- 0958-0670 (ISSN-L)
- 1469-445X
- OpenAlex
- W2504673739
- Cited by
- 16
- References
- 28
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 1 · 2023: 2 · 2022: 1 · 2021: 1 · 2019: 2 · 2018: 2 · 2017: 2 · 2016: 1
- FWCI
- 1.88
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Experimental Physiology (publishedVersion)
- PubMed (publishedVersion)
- Figshare (submittedVersion, cc-by-nc-nd)
- Leicester Research Archive (University of Leicester) (submittedVersion, cc-by-nc-nd)
- Funders
- University of Leicester
- Topics
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
- Keywords
- circadian rhythm, diurnal variation, endothelial nitric oxide synthase, nitric oxide signaling, vascular contractility, mesenteric arteries, vasoconstriction, vasodilation, acetylcholine, phenylephrine, alpha1-adrenoceptors, muscarinic receptors, sympathetic activity, blood pressure, peripheral circadian clock
- MeSH terms
- Animals, Blood Pressure, Endothelium, Vascular, Humans, Mesenteric Arteries, Vasoconstriction, Signal Transduction, Nitric Oxide Synthase Type III
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