Nitric oxide and sleep quality -
These findings are consistent with the hypothesis that nitric oxide may have arousal-promoting effects, mediated in part by the suprachiasmatic nucleus. In terms of the homeostatic process of sleep regulation, systemic injection of a nitric oxide synthase inhibitor shortened in length and decreased in amplitude the sleep rebound to sleep deprivation.
Also, in response to sleep deprivation, nitric oxide synthase enzyme activity was decreased in brain nuclei involved in sleep-wake cycle regulation. On the other hand, nitric oxide synthase protein amounts were increased following extended wakefulness, especially inducible nitric oxide synthase in the basal forebrain.
Systemic injection of a nitric oxide synthase inhibitor at a time when homeostatic sleep pressure is spontaneously highest, at light onset, also decreased sleep amounts, suggesting that and intact nitric oxide-ergic signaling cascade is necessary for proper sleep responses to be mounted after both spontaneous and forced wakefulness.
In addition, preliminary studies support the hypothesis that cyclic guanosine monophosphate could be a signaling molecule involved in carrying out at least part of the sleep-modulatory actions of nitric oxide.
Ribeiro, Ana Cristina, "The role of nitric oxide in physiological sleep regulation" ETD Collection for Fordham University. Am J Rhinol ;— Miljeteig H, Savard P, Mateika S, Cole P, Haight JSJ, HoffsteinV.
Snoring and nasal resistance during sleep. Cannon 3rdRO, Schechter AN, Panza JA, et al. Effects of inhaled nitric oxide on regional blood flow are consistent with intravascular nitric oxide delivery. J Clin Invest ;— Rossaint R, Falke KJ, Lopez F, Slama K, Pison U, ZapolWM.
Inhaled nitric oxide for adult respiratory distress syndrome [comment]. N Engl J Med ;— Klinger JR. Inhaled nitric oxide in ARDS. Crit Care Clin ;— Singh S, EvansTW. Nitric oxide the biological mediator of the decade: fact or fiction?.
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Myers JL, Wizorek JJ, Myers AK, et al. Maturation alters the pulmonary arterial response to hypoxia and inhaled nitric oxide in the presence of endothelial dysfunction. J Thorac Cardiovasc Surg ;— Kobzik L, ReidMB, Bredt DS, Stamler JS. Nitric oxide in skeletal muscle.
CAS PubMed Google Scholar. Murrant CL, Woodley NE, Barclay JK. Effect of nitroprusside and endothelium derived products on slow-twitch skeletal muscle function in vitro. Can J Physiol Pharmacol ;— Morrison RJ, Miller IIICC, Reid MB.
Nitric oxide effects on shortening velocity and power production in the rat diaphragm. J Appl Physiol ;— Nitric oxide effects on force-velocity characteristics of the rat diaphragm. Comp Biochem Physiol ;— Gath I, Closs EI, Godtel-ArmbrustU, et al.
Expressed in different structures of guinea-pig skeletal muscle: implications for contractile function. FASEB J ;— Reid MB. Role of nitric oxide in skeletal muscle: synthesis, distribution and functional importance.
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Arginine metabolism and the synthesis of nitric oxide in the nervous system. Prog Neurobiol ;— Blanchard AR, Chaudhary BA. Neuropharmacology of sleep and wakefulness. In: Lee-Chiong TL, Sateira MJ, Carskadon MA eds. Sleep Medicine.
Leonard TO, Lydic R. Pontine nitric oxide modulates acetylcholine release rapid eye movement sleep generation and respiratory rate. J Neurosci ;— Seigel JM. Brainstem mechanisms generating REM sleep. In: Kryger M, Roth T, Dement WC, eds. Philadelphia, PA: WB Saunders;; — Lai YY, Seigel JM.
Medullary regions mediating atonia. Datta S, PattersonEH, Siwek DF. Endogenous and exogenous nitric oxide in the pedunculo-pontine tegmentum induces sleep. Synapse ;— Muscle tone suppression and stepping produced by stimulation of midbrain and rostral pontine reticular formation.
Ponto-medullary glutamate receptors mediating locomotion and muscle tone suppression. Prast H, Tran MH, FischerH, Philippu A. Nitric oxide induced release of acetycholine in the nucleus accumbens: role of cyclic GMP, glutamate and GABA.
J Neurochem ;— Kimura T, Yu JG, Edvinsson L, LeeTJF. Cholinergic nitric oxide innervation in cerebral arteries of the cat. Bach-y-Rita P. Nonsynaptic diffusion neurotransmission NDN in the brain. Neurochem Int ;— Liu X, Miller MJ, Joshi MS, Sadowska-Krowicka H, Clark DA, Lancaster JrJR.
Diffusion-limited reaction of free nitric oxide with erythrocytes. J Biol Chem ;— Sippel JM, Giraud GD, Holden WE. Nasal administration of the nitric oxide synthase inhibitor L-NAME induces daytime somnolence. Cespuglio R, Burlet S, Marinesco S, Robert F, Jouvet M.
Volumetric detection of cerebral NO in rats. Variations of the signal throughout the sleep-wakefulness cycle. C R Acad Sci III ;— Kato M, Roberts, Thomson P, et al. Impairment of endothelium dependent vasodilation of resistance vessels in patients with obstructive sleep apnea.
Shepard JrJW, Garrison MW, Grither DA, et al. Relationship of ventricular ectopy to nocturnal oxygen desaturation in patients with chronic obstructive pulmonary disease. Am J Med ;— Butkov N. Atlas of Clinical PolysomngraphySynapse Media Inc; Haight JSJ, Qian W. Hypoxia depresses nitric oxide output in the human nasal airway.
Duchna HW, Guilleminault C, StoohsRA, et al. Obstructive sleep apnea syndrome: a cardiovascular risk factor?. Zschr Kardiol ;— Ip MS, Lam B, ChanLY, et al. Circulating nitric oxide is suppressed in obstructive sleep apnea and is reversed by nasal continuous positive airway pressure.
Am J Respir Crit Care ;— Schulz R, Schmidt D, Blum A, et al. Decreased plasma levels of nitric oxide derivatives in obstructive sleep apnoea: response to CPAP therapy. Thorax ;— McQuillan LP, Leung GK, Marsden PA, Kostyk SK, Kourembanas S.
Hypoxia inhibits expression of eNOS via transcriptional and post-transcriptional mechanisms. Am J Physiol ; 5 Pt 2 :H— Carlson J, Hedner J, Pettersson A. Increased plasma concentration of ADMA, a naturally occurring nitric oxide synthesis inhibitor, in OSA patients.
Am J Respir Crit Care ;A—A Schulz R, Seeger W, Grimminger F. Lavery CE, Mittleman MA, Cohen MC, et al. Within the laterodorsal tegmentum LDT , pedunculopontine tegmentum and dorsal raphe nucleus, NOS-containing neurons overlap neurons grouped according to their contribution to sleep mechanisms.
The main target for NO is the soluble guanylate cyclase that triggers an overproduction of cyclic guanosine monophosphate. NO in neurons of the pontine tegmentum facilitates sleep particularly rapid-eye-movement sleep , and NO contained within the LDT intervenes in modulating the discharge of the neurons through an auto-inhibitory process involving the co-synthesized neurotransmitters.
Moreover, NO synthesized within cholinergic neurons of the basal forebrain, while under control of the LDT, may modulate the spectral components of the EEG instead of the amounts of different sleep states.
Energy and performance optimization sleep quality qualkty duration are associated with systemic endothelial sleel. However, an association between poor sleep and pulmonary endothelial dysfunction has not been Nitric oxide and sleep quality. Oxidr sought to determine if there is a relationship between sleep duration and fractional exhaled nitric oxide FeNO concentrations as a surrogate for pulmonary endothelial function. We used three National Health and Nutrition Examination Survey NHANES cycles — To examine a non-linear relationship, we introduced a spline, with single knot at mean sleep duration 7 h.Metabolic health research Cristina RibeiroFordham University. Nitric oxide is a free radical neurotransmitter that qaulity involved in quakity Nitric oxide and sleep quality of physiological and pathological processes.
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On the other qualiyt, when the microinjections were aimed at the suprachiasmatic nucleus, nitric oxide donor suppressed rapid-eye-movement sleep. Systemic injection of a nitric oxide synthase inhibitor at dark-onset greatly increased rapid-eye-movement sleep.
These findings are consistent with the hypothesis that nitric oxide may have arousal-promoting effects, mediated in part by the suprachiasmatic nucleus. In terms of the homeostatic process of sleep regulation, systemic injection of a nitric oxide synthase inhibitor shortened in length and decreased in amplitude the sleep rebound to sleep deprivation.
Also, in response to sleep deprivation, nitric oxide synthase enzyme activity was decreased in brain nuclei involved in sleep-wake cycle regulation. On the other hand, nitric oxide synthase protein amounts were increased following extended wakefulness, especially inducible nitric oxide synthase in the basal forebrain.
Systemic injection of a nitric oxide synthase inhibitor at a time when homeostatic sleep pressure is spontaneously highest, at light onset, also decreased sleep amounts, suggesting that and intact nitric oxide-ergic signaling cascade is necessary for proper sleep responses to be mounted after both spontaneous and forced wakefulness.
In addition, preliminary studies support the hypothesis that cyclic guanosine monophosphate could be a signaling molecule involved in carrying out at least part of the sleep-modulatory actions of nitric oxide.
Ribeiro, Ana Cristina, "The role of nitric oxide in physiological sleep regulation" ETD Collection for Fordham University. Advanced Search. Home About FAQ My Account Accessibility Statement. Privacy Copyright. Skip to main content. Home About FAQ My Account. The role of nitric oxide in physiological sleep regulation Ana Cristina RibeiroFordham University Abstract Nitric oxide is a free radical neurotransmitter that is involved in a number of physiological and pathological processes.
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: Nitric oxide and sleep quality| Nitric oxide and sleep | Seigel JM. Reprints and permissions. Anterior diencephalic microinjection of a nitric oxide synthase inhibitor greatly increased rapid-eye-movement sleep, and these effects were also seen after sub-paraventricular zone microinjection of the nitric oxide synthase inhibitor. BMC Cardiovascular Disord. Department of Otorhinolaryngology, St. J Neurochem ;— Google Scholar Kimura T, Yu JG, Edvinsson L, LeeTJF. Protein expression and phosphorylation of eNOS in the aortas of middle-aged rats. |
| The effect of sleep duration on exhaled nitric oxide levels in U.S. adults | Sleep and Breathing | Evidence from a canine model. Informed consent was obtained from all individual participants included in the study. Abstract Nitric oxide NO and obstructive sleep apnea are inseparable. Access this article Log in via an institution. Sleep Data from Over , People Reveal Global Differences in Weekly Sleep Variability and Sleep Extension. |
| "The role of nitric oxide in physiological sleep regulation" by Ana Cristina Ribeiro | Within the laterodorsal tegmentum LDT , pedunculopontine tegmentum and dorsal raphe nucleus, NOS-containing neurons overlap neurons grouped according to their contribution to sleep mechanisms. The main target for NO is the soluble guanylate cyclase that triggers an overproduction of cyclic guanosine monophosphate. NO in neurons of the pontine tegmentum facilitates sleep particularly rapid-eye-movement sleep , and NO contained within the LDT intervenes in modulating the discharge of the neurons through an auto-inhibitory process involving the co-synthesized neurotransmitters. Moreover, NO synthesized within cholinergic neurons of the basal forebrain, while under control of the LDT, may modulate the spectral components of the EEG instead of the amounts of different sleep states. We studied whether endothelial dysfunction also existed in REM sleep deprivation-induced hypertension. The results showed that endothelium-dependent vasorelaxation was decreased significantly in middle-aged rats with REM sleep deprivation Fig 2 ; this change was due to impaired NO production Fig 3A. In the blood vessel wall, NO is produced mainly from L-arginine by the enzyme eNOS and regulates the degree of contraction of vascular smooth muscle cells mainly by stimulating soluble guanylyl cyclase sGC to produce cGMP[ 18 ]. Given that exogenous L-arginine supplementation can ameliorate the development of hypertension in rats[ 19 — 21 ], we next observed the effects of L-arginine on REM sleep deprivation-induced pathological changes in middle-aged rats. In this study, we treated REM sleep deprivation with L-arginine in drinking water. As expected, L-arginine supplementation could increase eNOS phosphorylation Fig 5 , augment NO and cGMP production Fig 4 , improve NO-mediated vasodilation Figs 2B and 3A , and consequently decrease blood pressure Fig 1D. Interestingly, L-arginine supplementation can protect against REM sleep deprivation-induced endothelial dysfunction and hypertension. In addition, the study results also indicate that endothelial dysfunction due to damaged NO bioavailability contributes to REM sleep deprivation-induced hypertension. Given that there are many adverse side effects of the long-term usage of insomnia medications to improve insomnia or increase sleep duration[ 22 ], it is difficult to suppress sleep loss-induced adverse effects on the cardiovascular system. The present study provides a new strategy for inhibiting the signaling pathways that contribute to insomnia-induced or insomnia-enhanced cardiovascular diseases. However, the present study was performed in SD rats. It is unclear if other rat strains also have similar response to REM sleep deprivation. Different rat strains may have different responses given different genetic makeup. Further study is needed to understand this question. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Article Authors Metrics Comments Media Coverage Reader Comments Figures. Abstract Sleep loss can induce or aggravate the development of cardiovascular and cerebrovascular diseases. Introduction Sleep is essential for an individual's mental, emotional, and physiological well-being. Materials and methods Animals Six-week-old young and week-old middle-aged male Sprague-Dawley rats were purchased from Shanghai Slack Laboratory Animal Co. REM sleep deprivation Animals were deprived of sleep via the disk-over-water method, with certain modifications[ 10 ]. Blood pressure measurement Rats were anesthetized with isoflurane. Myograph study Rats were sacrificed, and the descending thoracic aorta was harvested. NO assay NO production in situ is difficult to detect because of its rapid decay within seconds in physiological systems. Statistical analysis All data were expressed as means±SEM, and n refers to the number of rats. Results Effects of REM sleep deprivation on body weight and blood pressure REM sleep deprivation caused significant reductions in body weight in young and middle-aged rats Fig 1A and 1B. Download: PPT. Fig 1. Body weights and blood pressures with or without REM sleep deprivation REMSD. Effects of REM sleep deprivation on endothelial function REM sleep deprivation did not affect ACh-mediated vasodilatation in the aortas of young rats Fig 2A. Fig 2. Acetylcholine ACh -induced vasorelaxation of the aortas of rats. Fig 3. Different channel mediated vasorelaxation of the aortas of middle-aged rats. Effects of REM sleep deprivation on NO and cGMP concentrations in middle-aged rats As shown in Fig 4 , REM sleep deprivation decreased NO production and cGMP levels in the aortas of middle-aged rats. Fig 4. NO production and cGMP concentration in the aortas of middle-aged rats. Effects of REM sleep deprivation on eNOS expression in middle-aged rats Western blotting revealed decreased expression of the phosphorylated eNOS protein in REM sleep-deprived rats. Fig 5. Protein expression and phosphorylation of eNOS in the aortas of middle-aged rats. Supporting information. S1 File. Data availability statement. Important data of figures in the article. s PDF. S2 File. ARRIVE guidelines checklist. References 1. Altman NG, Izci-Balserak B, Schopfer E, Jackson N, Rattanaumpawan P, Gehrman PR,et al. Sleep duration versus sleep insufficiency as predictors of cardiometabolic health outcomes. Sleep Med. Vgontzas AN, Liao D, Bixler EO, Chrousos GP and Vela-Bueno A. Insomnia with objective short sleep duration is associated with a high risk for hypertension. Li Y, Vgontzas AN, Fernandez-Mendoza J, Bixler EO, Sun YF, Zhou JY,et al. Insomnia with physiological hyperarousal is associated with hypertension. Palagini L, Maria Bruno R, Gemignani A, Baglioni C, Ghiadoni L, Dieter R. Sleep Loss and Hypertension: A Systematic Review. Curr Pharm Des. Yolanda M, Silvia L, and Eduardo N. Reactivity of the aorta and mesenteric resistance arteries from the obese spontaneously hypertensive rat: effects of glitazones. Am J Physiol Heart Circ Physiol. Kensuke E. Clinical Importance of Endothelial Function in Arteriosclerosis and Ischemic Heart Disease. Circ J. Sauvet F, Florence G, Van Beers P, Drogou C, Lagrume C, Chaumes C,et al. Total sleep deprivation alters endothelial function in rats: a nonsympathetic mechanism. Calvin AD, Covassin N, Kremers WK, Adachi T, Macedo P,Albuquerque FN,et al. Experimental sleep restriction causes endothelial dysfunction in healthy humans. To examine the role of nitric oxide in the circadian component of sleep regulation, nitric oxide donors and a nitric oxide synthase inhibitor were microinjected directly to the suprachiasmatic nucleus, a major output of the suprachiasmatic nucleus, the sub-paraventricular zone, or the area surrounding the circadian pacemaker diencephalic region and sleep responses were recorded. Anterior diencephalic microinjection of a nitric oxide synthase inhibitor greatly increased rapid-eye-movement sleep, and these effects were also seen after sub-paraventricular zone microinjection of the nitric oxide synthase inhibitor. On the other hand, when the microinjections were aimed at the suprachiasmatic nucleus, nitric oxide donor suppressed rapid-eye-movement sleep. Systemic injection of a nitric oxide synthase inhibitor at dark-onset greatly increased rapid-eye-movement sleep. These findings are consistent with the hypothesis that nitric oxide may have arousal-promoting effects, mediated in part by the suprachiasmatic nucleus. In terms of the homeostatic process of sleep regulation, systemic injection of a nitric oxide synthase inhibitor shortened in length and decreased in amplitude the sleep rebound to sleep deprivation. Also, in response to sleep deprivation, nitric oxide synthase enzyme activity was decreased in brain nuclei involved in sleep-wake cycle regulation. On the other hand, nitric oxide synthase protein amounts were increased following extended wakefulness, especially inducible nitric oxide synthase in the basal forebrain. |
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