Short Sleep Duration is Associated with Enhanced Endothelin-1 vasoconstrictor tone.

Document Type

Article

Publication Date

8-1-2010

Abstract

Short sleep duration is associated with increased cardiovascular disease (CVD) morbidity. Endothelial vasomotor dysfunction represents a potential mechanism contributing to the increased CVD risk associated with habitual short sleep duration. Endothelin (ET)-1 is a potent vasoconstrictor peptide that is associated with endothelial vasomotor dysfunction and increased CVD risk. Currently, there is no information regarding the influence of short sleep duration on ET-1 vasoconstrictor activity in adults. We tested the hypothesis that ET-1-mediated vasoconstrictor activity is greater in adults who sleep less than 7 h/night (short sleep duration) compared with those who sleep 7-9 h/night (normal sleep duration). Forearm blood flow (FBF) responses to intra-arterial infusion of BQ-123 (100 nmol/min for 60 min), a selective ETA receptor antagonist, were determined in 80 adults: 50 with normal sleep duration (32 males and 18 females; age: 56.6 +/- 1.2 years; sleep: 7.6 +/- 0.1 h/night) and 30 with short sleep duration (17 males and 13 females; age: 56.5 +/- 1.2 years; sleep: 6.1 +/- 0.1 h/night). In response to BQ-123, adults reporting short sleep duration had a greater increase in resting FBF compared with adults reporting normal sleep duration (approximately 20% vs. approximately 8%; P < 0.05). There was an inverse relation between mean nightly sleep duration and the FBF response to BQ-123 at 60 min (r = -0.29, P < 0.05). These findings indicate that habitual short sleep duration is associated with greater ET-1-mediated vasoconstrictor tone. Increased ET-1 vasoconstrictor activity may contribute to the elevated CVD risk associated with chronic reductions in sleep duration.

Publication Title

Canadian Journal of Physiology and Pharmacology

Volume

88

Issue

8

First Page

777

Last Page

781

DOI of Published Version

10.1139/Y10-046

Publisher

NRC Research Press

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