Influence of exogenous melatonin on catecholamine levels in postmenopausal women prior and during oestradiol replacement

Cagnacci, Angelo; Zanni, Anna Lisa; Veneri, Maria Grazia; Menozzi, Renata; Volpe, Annibale; Rió, G. Del

doi:10.1046/j.1365-2265.2000.01099.x

Cited by 14 publications

(16 citation statements)

References 35 publications

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“…Arangino and co-workers [24] showed that a single administration of 1 mg melatonin administration in healthy male subjects between 2:30 and 5:30 PM reduced BP, norepinephrine levels, and pulsatility index in the internal carotid artery (PI; as measure of vascular reactivity) compared to placebo administration. Cagnacci and co-workers [103] showed a reduction of systolic and diastolic BP and PI by a single daytime melatonin dose also in menopausal women with hormonal replacement therapy. However, a potential concern with daytime melatonin administration is that melatonin induces sleepiness, which most likely is an unwanted side-effect in the treatment of high BP or HR.…”

Section: The Cardiovascular System and Melatoninmentioning

confidence: 99%

Effects of circadian disruption on the cardiometabolic system

Rüger

Scheer

2009

Rev Endocr Metab Disord

194

142

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The presence of day-night variations in cardiovascular and metabolic functioning is well known. However, only recently it has been shown that cardiovascular and metabolic processes are not only affected by the behavioral sleep/wake cycle but are partly under direct control of the master circadian pacemaker located in the suprachiasmatic nucleus (SCN). Heart rate, cardiac autonomic activity, glucose metabolism and leptin -involved in appetite control-all show circadian variation (i.e., under constant behavioral and environmental conditions). This knowledge of behavioral vs. circadian modulation of cardiometabolic function is of clinical relevance given the morning peak in adverse cardiovascular incidents observed in epidemiological studies and given the increased risk for the development of diabetes, obesity, and cardiovascular disease in shift workers. We will review the evidence for circadian control of cardiometabolic functioning, as well its sensitivity to light and melatonin, and discuss potential implication for therapy.

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Section: The Cardiovascular System and Melatoninmentioning

confidence: 99%

Effects of circadian disruption on the cardiometabolic system

Rüger

Scheer

2009

Rev Endocr Metab Disord

194

142

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“…Also a marker of bone formation such as serum bone alkaline phosphatase activity, as well as serum phosphorus levels, augmented in melatonin‐treated rats at an early time after ovariectomy [12]. As appropriate circulating oestradiol levels could be needed for melatonin effects on bone, as they are for some biological responses to melatonin in women [13], the present study was undertaken to assess whether oestradiol replacement in ovariectomized rats prolongs the response to melatonin after ovariectomy. Recently, two publications in abstract form also provided evidence on the preventing effect of melatonin on bone loss [14, 15].…”

Section: Introductionmentioning

confidence: 99%

Melatonin increases oestradiol‐induced bone formation in ovariectomized rats

Ladizesky

Boggio

Albornoz

et al. 2003

Journal of Pineal Research

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: To assess the effect of melatonin on bone metabolism in ovariectomized rats, receiving oestradiol therapy or not, melatonin was administered in the drinking water (25 μg/mL water) and oestradiol (10 μg/kg body weight) or vehicle was given subcutaneously 5 days/week for up to 60 days after surgery. Urinary deoxypyridinoline (a marker of bone resorption) and circulating levels of bone alkaline phosphatase activity (a marker of bone formation), as well as serum calcium and phosphorus levels, were measured every 15 days. Bone area (BA), bone mineral content (BMC), bone mineral density (BMD) and total body fat (expressed as 100 g body weight) were measured by dual‐energy X‐ray absorptiometry at the end of the experiment. Body weight and total body fat were augmented after ovariectomy, and decreased after melatonin or oestradiol treatment. The effect of melatonin on body weight was seen in sham‐operated rats only. Ovariectomy augmented, and melatonin or oestradiol lowered, urinary deoxypyridinoline excretion. This effect of melatonin and oestradiol was seen mainly in ovariectomized rats. The efficacy of oestradiol to counteract ovariectomy‐induced bone resorption was increased by melatonin. Melatonin or oestradiol lowered serum bone alkaline phosphatase activity. Melatonin inhibition was seen mainly on the increase of bone alkaline phosphatase activity that followed ovariectomy. Serum phosphorus levels decreased after melatonin administration and were augmented after oestradiol injection; overall, melatonin impaired the increase of serum phosphorus caused by oestradiol. Ovariectomy decreased, and oestradiol increased, serum calcium levels while melatonin augmented serum calcium in sham‐operated rats only. On day 60 after surgery, BMD and content decreased after ovariectomy and were increased after oestradiol injection. Melatonin augmented BA of spine and BMC of whole of the skeleton and tibia. The highest values observed were those of rats treated concurrently with oestradiol and melatonin. The present results indicate that: (i) melatonin treatment restrained bone remodelling after ovariectomy; (ii) the effect of melatonin required adequate concentrations of oestradiol; (iii) melatonin augmented oestradiol effects on bone in ovariectomized rats; (iv) a counter‐regulation by melatonin of the increase in body fat caused by ovariectomy was uncovered. The melatonin doses employed were pharmacological in terms of circulating melatonin levels but not necessarily for some other fluids or tissues.

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“…Whether a similar differential modulation of melatonin receptors by HRT is operative also in postmenopausal women is presently unknown. On the other hand, we have recently reported that the capability of melatonin to influence noradrenergic activity in humans is modulated by gonadal steroids: HRT allows the maximal inhibitory effect of melatonin on basal and stimulated norepinephrine levels (Cagnacci et al . 2000).…”

Section: Discussionmentioning

confidence: 99%