Daily Melatonin Administration Attenuates Age-Dependent Disturbances of Cardiovascular Rhythms

Gubin, Denis; Губин, Г. Д.; Gapon, L.; Weinert, Dietmar

doi:10.2174/1874609809666151130220011

Cited by 53 publications

(25 citation statements)

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“…Furthermore, circadian dysfunction accelerates cellular aging and mortality with period alterations shortening lifespan in animal models (Krishnan et al, 2012, Park et al, 2012). The decline in the robustness of the circadian system appears to arise earlier in peripheral tissues than the central brain (Gubin et al, 2016, Libert et al, 2012) underscoring the need for examination of circadian processes during middle age. Given the circadian modulation of alcohol-induced behaviors and toxicity, the need exists for a tractable model suitable for dual examination of the circadian clock and alcohol neurobiology across multiple age groups.…”

Section: Introductionmentioning

confidence: 99%

Aging and circadian dysfunction increase alcohol sensitivity and exacerbate mortality in Drosophila melanogaster

Nobrega

Mellers

Lyons

2017

Experimental Gerontology

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Alcohol abuse is a rising problem in middle-aged and older individuals resulting in serious health, family and economic consequences. Effective treatment necessitates the identification of factors influencing alcohol toxicity with aging. We investigated the interaction between aging, alcohol toxicity and circadian function using Drosophila as a model system. We found as wild type flies age, sensitivity to alcohol increases and circadian regulation of alcohol-induced behaviors weakens. Decreased circadian modulation is correlated with significantly greater alcohol sensitivity during the subjective day. The circadian clock modulates alcohol-induced mortality in younger flies with increased mortality following alcohol exposure at night. Older flies exhibit significantly longer recovery times following alcohol-induced sedation and increased mortality following binge-like or chronic alcohol exposure. Flies rendered arrhythmic either genetically or environmentally exhibit significantly increased alcohol sensitivity, longer recovery times and increased mortality. We hypothesize that the circadian clock phase specifically buffers behavioral and cellular alcohol sensitivity with this protection diminishing as the circadian clock weakens with age.

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Section: Introductionmentioning

confidence: 99%

Aging and circadian dysfunction increase alcohol sensitivity and exacerbate mortality in Drosophila melanogaster

Nobrega

Mellers

Lyons

2017

Experimental Gerontology

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“…Cry1 and Cry2-deficient mice are prone to salt sensitive hypertension due to increased activity of the adrenocortical aldosterone-producing enzyme, 3 beta-hydroxyl-steroid dehydrogenase (111). Recent studies also suggest that melatonin has multiple beneficial effects on the cardiovascular system; melatonin administration at bedtime reduces blood pressure in hypertensive patients (112). Thus, it is possible that alterations in circadian rhythm may affect melatonin levels resulting in autonomic nervous dysfunction, increased aldosterone, and subsequent hypertension.…”

Section: Hypothalamic Mechanisms Of Hypertensionmentioning

confidence: 99%

Hypothalamic and inflammatory basis of hypertension

Khor

Cai

2017

Clinical Science

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Hypertension is a major health problem with great consequences for public health. Despite its role as the primary cause of significant morbidity and mortality associated with cardiovascular disease, the pathogenesis of essential hypertension remains largely unknown. The central nervous system in general, and the hypothalamus in particular, are intricately involved in the development and maintenance of hypertension. Over the last several decades, the understanding of the brain’s role in the development of hypertension has dramatically increased. This brief review is to summarize the neural mechanisms of hypertension with a focus on neuroendocrine and neurotransmitter involvement, highlighting recent findings which suggest that hypothalamic inflammation disrupts key signaling pathways to affect the central control of blood pressure, and therefore suggesting future development of interventional strategies that exploit recent findings pertaining to the hypothalamic control of blood pressure as well as the inflammatory-sympathetic mechanisms involved in hypertension.

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“…In 26 healthy awake men, 2 mg of melatonin was administered in the supine position and after 60 min a decrease of HR and BP, an increase of HR variability, and a drop in plasma norepinephrine and dopamine were observed in comparison with placebo‐injected subjects . In 97 normotensive and hypertensive elderly volunteers, administration of 1.5 mg of melatonin for 2 weeks at the bedtime induced a reduction in systolic and diastolic BP and attenuation of HR increase between 0300 and 0800 h in the morning, that is, at the time of the highest cardiovascular risk . Recently, a study involving 78 patients with postural tachycardia syndrome showed that melatonin caused a significantly greater reduction in standing HR two hours after melatonin administration compared to placebo …”

Section: Melatonin As a Potential Means Of Hr Reduction In Hypertensionmentioning

confidence: 99%

Elevated heart rate and nondipping heart rate as potential targets for melatonin: a review

Šimko¹,

Baka²,

Paulis³

et al. 2016

Journal of Pineal Research

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Elevated heart rate is a risk factor for cardiovascular and all‐cause mortalities in the general population and various cardiovascular pathologies. Insufficient heart rate decline during the night, that is, nondipping heart rate, also increases cardiovascular risk. Abnormal heart rate reflects an autonomic nervous system imbalance in terms of relative dominance of sympathetic tone. There are only a few prospective studies concerning the effect of heart rate reduction in coronary heart disease and heart failure. In hypertensive patients, retrospective analyses show no additional benefit of slowing down the heart rate by beta‐blockade to blood pressure reduction. Melatonin, a secretory product of the pineal gland, has several attributes, which predict melatonin to be a promising candidate in the struggle against elevated heart rate and its consequences in the hypertensive population. First, melatonin production depends on the sympathetic stimulation of the pineal gland. On the other hand, melatonin inhibits the sympathetic system in several ways representing potentially the counter‐regulatory mechanism to normalize excessive sympathetic drive. Second, administration of melatonin reduces heart rate in animals and humans. Third, the chronobiological action of melatonin may normalize the insufficient nocturnal decline of heart rate. Moreover, melatonin reduces the development of endothelial dysfunction and atherosclerosis, which are considered a crucial pathophysiological disorder of increased heart rate and pulsatile blood flow. The antihypertensive and antiremodeling action of melatonin along with its beneficial effects on lipid profile and insulin resistance may be of additional benefit. A clinical trial investigating melatonin actions in hypertensive patients with increased heart rate is warranted.

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Daily Melatonin Administration Attenuates Age-Dependent Disturbances of Cardiovascular Rhythms

Cited by 53 publications

References 0 publications

Aging and circadian dysfunction increase alcohol sensitivity and exacerbate mortality in Drosophila melanogaster

Aging and circadian dysfunction increase alcohol sensitivity and exacerbate mortality in Drosophila melanogaster

Hypothalamic and inflammatory basis of hypertension

Elevated heart rate and nondipping heart rate as potential targets for melatonin: a review

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