STUDY OBJECTIVES: Sleep loss is suspected to induce endothelial dysfunction, a key factor in cardiovascular risk. We examined whether sympathetic activity is involved in the endothelial dysfunction caused by total sleep deprivation (TSD). DESIGN: TWO GROUPS: TSD (24-h wakefulness), using slowly rotating wheels, and wheel control (WC). PARTICIPANTS: Seven-month-old male Wistar rats. INTERVENTIONS: Pharmacological sympathectomy (reserpine, 5 mg/kg, intraperitoneal), nitric oxide synthase (NOS) inhibition (N (G)-nitro-L-arginine, 20 mg/kg, intraperitoneally 30 min before experiment) and cyclooxygenase (COX) inhibition (indomethacin, 5 mg/kg, intraperitoneally 30 min before experiment). MEASUREMENTS AND RESULTS: In protocol 1, changes in heart rate (HR) and blood pressure were continuously recorded in the sympathectomized and non-sympathectomized rats. Blood pressure and HR increased during TSD in non-sympathectomized rats. In protocol 2, changes in skin blood flow (vasodilation) were assessed in the sympathectomized and non-sympathectomized rats using laser-Doppler flowmetry coupled with iontophoretic delivery of acetylcholine (ACh), sodium nitroprusside (SNP), and anodal and cathodal currents. ACh- and cathodal current-induced vasodilations were significantly attenuated after TSD in non-sympathectomized and sympathectomized rats (51% and 60%, respectively). In protocol 3, ACh-induced vasodilation was attenuated after NOS and COX inhibition (66% and 49%, respectively). Cathodal current-induced vasodilation decreased by 40% after COX inhibition. In TSD compared to WC a decrease in ACh-induced vasodilation was still observed after COX inhibition. No changes in SNP- and anodal current-induced vasodilation were detected. CONCLUSION: These results demonstrate that total sleep deprivation induces a reduction in endothelial-dependent vasodilation. This endothelial dysfunction is independent of blood pressure and sympathetic activity but associated with nitric oxide synthase and cyclooxygenase pathway alterations.
STUDY OBJECTIVES: Sleep loss is suspected to induce endothelial dysfunction, a key factor in cardiovascular risk. We examined whether sympathetic activity is involved in the endothelial dysfunction caused by total sleep deprivation (TSD). DESIGN: TWO GROUPS: TSD (24-h wakefulness), using slowly rotating wheels, and wheel control (WC). PARTICIPANTS: Seven-month-old male Wistar rats. INTERVENTIONS: Pharmacological sympathectomy (reserpine, 5 mg/kg, intraperitoneal), nitric oxide synthase (NOS) inhibition (N (G)-nitro-L-arginine, 20 mg/kg, intraperitoneally 30 min before experiment) and cyclooxygenase (COX) inhibition (indomethacin, 5 mg/kg, intraperitoneally 30 min before experiment). MEASUREMENTS AND RESULTS: In protocol 1, changes in heart rate (HR) and blood pressure were continuously recorded in the sympathectomized and non-sympathectomized rats. Blood pressure and HR increased during TSD in non-sympathectomized rats. In protocol 2, changes in skin blood flow (vasodilation) were assessed in the sympathectomized and non-sympathectomized rats using laser-Doppler flowmetry coupled with iontophoretic delivery of acetylcholine (ACh), sodium nitroprusside (SNP), and anodal and cathodal currents. ACh- and cathodal current-induced vasodilations were significantly attenuated after TSD in non-sympathectomized and sympathectomized rats (51% and 60%, respectively). In protocol 3, ACh-induced vasodilation was attenuated after NOS and COX inhibition (66% and 49%, respectively). Cathodal current-induced vasodilation decreased by 40% after COX inhibition. In TSD compared to WC a decrease in ACh-induced vasodilation was still observed after COX inhibition. No changes in SNP- and anodal current-induced vasodilation were detected. CONCLUSION: These results demonstrate that total sleep deprivation induces a reduction in endothelial-dependent vasodilation. This endothelial dysfunction is independent of blood pressure and sympathetic activity but associated with nitric oxide synthase and cyclooxygenase pathway alterations.
Authors: Haythem Debbabi; Philippe Bonnin; Pierre Henri Ducluzeau; Georges Lefthériotis; Bernard I Levy Journal: Am J Hypertens Date: 2010-02-18 Impact factor: 2.689
Authors: Coralie Zegre Cannon; Grace E Kissling; David R Goulding; Angela P King-Herbert; Terry Blankenship-Paris Journal: Lab Anim (NY) Date: 2011-03 Impact factor: 12.625
Authors: Hans K Meier-Ewert; Paul M Ridker; Nader Rifai; Meredith M Regan; Nick J Price; David F Dinges; Janet M Mullington Journal: J Am Coll Cardiol Date: 2004-02-18 Impact factor: 24.094
Authors: Martica H Hall; Suresh Mulukutla; Christopher E Kline; Laura B Samuelsson; Briana J Taylor; Julian F Thayer; Robert T Krafty; Ellen Frank; David J Kupfer Journal: Sleep Date: 2017-01-01 Impact factor: 5.849
Authors: Adam P Spira; Katie L Stone; Susan Redline; Kristine E Ensrud; Sonia Ancoli-Israel; Jane A Cauley; Kristine Yaffe Journal: Sleep Date: 2017-08-01 Impact factor: 5.849
Authors: Brandon P Lucke-Wold; Kelly E Smith; Linda Nguyen; Ryan C Turner; Aric F Logsdon; Garrett J Jackson; Jason D Huber; Charles L Rosen; Diane B Miller Journal: Neurosci Biobehav Rev Date: 2015-05-06 Impact factor: 8.989
Authors: M Chennaoui; D Gomez-Merino; C Drogou; H Geoffroy; G Dispersyn; C Langrume; S Ciret; T Gallopin; F Sauvet Journal: J Inflamm (Lond) Date: 2015-09-30 Impact factor: 4.981
Authors: G Hurtado-Alvarado; E Domínguez-Salazar; L Pavon; J Velázquez-Moctezuma; B Gómez-González Journal: J Immunol Res Date: 2016-09-21 Impact factor: 4.818