In mammals, a central circadian clock, located in the suprachiasmatic nuclei (SCN) of the hypothalamus, tunes the innate circadian physiological rhythms to the ambient 24 h light-dark cycle to invigorate and optimize the internal temporal order. The SCN-activated, light-inhibited production of melatonin conveys the message of darkness to the clock and induces night-state physiological functions, for example, sleep/wake blood pressure and metabolism. Clinically meaningful effects of melatonin treatment have been demonstrated in placebo-controlled trials in humans, particularly in disorders associated with diminished or misaligned melatonin rhythms, for example, circadian rhythm-related sleep disorders, jet lag and shift work, insomnia in children with neurodevelopmental disorders, poor (non-restorative) sleep quality, non-dipping nocturnal blood pressure (nocturnal hypertension) and Alzheimer's disease (AD). The diminished production of melatonin at the very early stages of AD, the role of melatonin in the restorative value of sleep (perceived sleep quality) and its sleep-anticipating effects resulting in attenuated activation of certain brain networks are gaining a new perspective as the role of poor sleep quality in the build-up of β amyloid, particularly in the precuneus, is unravelled. As a result of the recently discovered relationship between circadian clock, sleep and neurodegeneration, new prospects of using melatonin for early intervention, to promote healthy physical and mental ageing, are of prime interest in view of the emerging link to the aetiology of Alzheimer's disease. LINKED ARTICLES: This article is part of a themed section on Recent Developments in Research of Melatonin and its Potential Therapeutic Applications. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.16/issuetoc.

https://bpspubs.onlinelibrary.wiley.com/doi/epdf/10.1111/bph.14116

New perspectives on the role of melatonin in human sleep, circadian rhythms and their regulation

Experimental studies have proven that melatonin has many beneficial pleiotropic actions. The aim of this study was to assess melatonin efficacy in patients with metabolic syndrome (MS). The study included 33 healthy volunteers (who were not treated with melatonin) and 30 patients with MS, who did not respond to 3-month lifestyle modification. Patients with MS were treated with melatonin (5 mg/day, 2 hr before bedtime) for 2 months. The following parameters were studied: systolic and diastolic blood pressure (SBP, DBP), levels of glucose, serum lipids, C-reactive protein, fibrinogen, activities of antioxidative enzymes: catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), thiobarbituric acid reactive substrates (TBARS). After 2-month therapy in comparison with baseline, the following significant changes were measured: systolic blood pressure (132.8±9.8 versus 120.5±11.0 mmHg, P<0.001), DBP (81.7±8.8 versus 75±7.4 mmHg, P<0.01), low-density lipoprotein cholesterol (LDL-C) (149.7±26.4 versus 139.9±30.2 mg/dL, P<0.05), TBARS (0.5±0.2 versus 0.4±0.1 μm/gHb, P<0.01), and CAT (245.9±46.9 versus 276.8±39.4 U/gHb). Melatonin administered for 2 months significantly improved antioxidative defense (increase in CAT activity, decrease in TBARS level) and lipid profile (decrease in LDL-C), and lowered blood pressure. We conclude that melatonin therapy may be of benefit for patients with MS, particularly with arterial hypertension. Further studies with higher doses of melatonin or prolonged supplementation are awaited.

Melatonin treatment improves blood pressure, lipid profile, and parameters of oxidative stress in patients with metabolic syndrome

Melatonin, acting through melatonin receptors, is involved in numerous physiological processes including circadian entrainment, blood pressure regulation, oncogenesis, retinal physiology, seasonal reproduction, ovarian physiology, immune function and most recently in inducing osteoblast differentiation. Moreover, melatonin was proved to be a potent-free radical scavenger and a broad-spectrum antioxidant. More research is required into the effects of therapeutically modulating the melatoninergic system on circadian haemodynamics and rhythm under varying physiopathological conditions and the possible impact on morbidity and mortality in humans.

Melatonin: therapeutic and clinical utilization

The number of patients with well-controlled hypertension is alarmingly low worldwide and new approaches to treatment of increased blood pressure (BP) are being sought. Melatonin has a role in blood pressure regulation. The nighttime production of melatonin is found to be reduced in hypertensive individuals. Administration of melatonin decreased BP in several animal models of hypertension, in healthy men and women, and in patients with arterial hypertension. Most promising results were achieved in patients with non-dipping nighttime pressure, in which the circadian rhythm of BP variation is disturbed. Several potential mechanisms of BP reduction are considered. Melatonin can, via its scavenging and antioxidant nature, improve endothelial function with increased availability of nitric oxide exerting vasodilatory and hypotensive effects. Melatonin seems to interfere with peripheral and central autonomic system, with a subsequent decrease in the tone of the adrenergic system and an increase of the cholinergic system. Melatonin may act on BP also via specific melatonin receptors localized in peripheral vessels or in parts of central nervous system participating in BP control. With a large clinical trial using melatonin in hypertension treatment, many important questions could be answered, such as the dose of melatonin and regimen of its application, the choice of patients with greatest possible benefit from melatonin treatment, the potential of anti-remodeling effect of melatonin and the interaction of melatonin with other antihypertensive drugs.

Melatonin as a potential antihypertensive treatment

Sleep is a neurochemical process involving sleep promoting and arousal centers in the brain. Sleep performs an essential restorative function and facilitates memory consolidation in humans. The remarkably standardized bouts of consolidated sleep at night and daytime wakefulness reflect an interaction between the homeostatic sleep need that is manifested by increase in sleep propensity after sleep deprivation and decrease during sleep and the circadian pacemaker. Melatonin, the hormone produced nocturnally by the pineal gland, serves as a time cue and sleep-anticipating signal. A close interaction exists between the sleep-wake, melatonin, core temperature, blood pressure, immune and hormonal rhythms leading to optimization of the internal temporal order. With age the robustness of the circadian system decreases and the prevalence of sleep disorders, particularly insomnia, increases. Deviant sleep patterns are associated with increased risks of morbidity, poor quality of life and mortality. Current sleep pharmacotherapies treat insufficient sleep quantity, but fail to improve daytime functioning. New treatment modalities for sleep disorders that will also improve daytime functioning remain a scientific and medical challenge.

Sleep and sleep disturbances: biological basis and clinical implications.

Plasma melatonin concentrations in hypertensive patients with the dipping and non-dipping blood pressure profile.

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Plasma melatonin concentrations in hypertensive patients with the dipping and non-dipping blood pressure profile.