Short sleep duration is associated with enhanced endothelin-1 vasoconstrictor tone.
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.
Weil
Brian R
BR
Integrative Vascular Biology Laboratory, Department of Integrative Physiology, University of Colorado, Boulder, CO 80309, USA.
Mestek
Michael L
ML
Westby
Christian M
CM
Van Guilder
Gary P
GP
Greiner
Jared J
JJ
Stauffer
Brian L
BL
DeSouza
Christopher A
CA
D000959:Antihypertensive Agents / Q000494:pharmacology; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1 / Q000037:antagonists & inhibitors / Q000378:metabolism*; D005260:Female; D005542:Forearm / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010456:Peptides, Cyclic / Q000494:pharmacology; D012039:Regional Blood Flow / Q000187:drug effects / Q000502:physiology; D012892:Sleep Deprivation / Q000503:physiopathology*; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
D000959:Antihypertensive Agents; D065128:Endothelin Receptor Antagonists; D019332:Endothelin-1; D010456:Peptides, Cyclic; C072247:cyclo(Trp-Asp-Pro-Val-Leu)