Impaired Basal Sympathetic Tone and α1-Adrenergic Responsiveness in Association With the Hypotensive Effect of Melatonin in Spontaneously Hypertensive Rats

Laflamme, Annik K.; Wu, Lin‐Sheng; Foucart, Sylvain; Champlain, Jacques de

doi:10.1016/s0895-7061(97)00401-9

Cited by 89 publications

(56 citation statements)

References 21 publications

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“…Spontaneously hypertensive rats (the animal model of arterial hypertension with the increased activity of the sympathetic system) are more sensitive to melatonin than are transgenic rats, TGR(mRen-2)27, with an upregulated renin-angiotensin-aldosterone system. 22 In our study, the etiology of arterial hypertension, which was present in the case of some patients, was also not known, but the differences in reaction to melatonin supplementation suggest that the group was not homogenous in this respect. Similar to our previous publication, no relationship was found between the effect of melatonin supplementation and the presence or accumulation of classical risk factors of ischemic heart disease nor between the kind of pharmacological treatment used.…”

Section: Study Limitationsmentioning

confidence: 62%

Melatonin for nondippers with coronary artery disease: assessment of blood pressure profile and heart rate variability

et al. 2009

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The aim of this study was to assess the effects of 5 mg melatonin before sleep in patients with coronary artery disease (CAD) and with an abnormal circadian pattern of blood pressure (BP) on changes in circadian BP profile and heart rate variability (HRV). Sixty patients with CAD, nondippers aged 48-80 years (male 75%), were included. In addition to previous treatment, they were randomly allocated to melatonin or placebo. After 90 days, a second 24-h BP monitoring was carried out. Each patient had two sessions (before randomization and at the end of study) of 24-h ECG monitoring to assess the changes in HRV. Inclusion of melatonin led to BP pattern normalization in 35% of patients in the melatonin group and in 15% of controls (P¼0.609). This effect was reached not only by a decrease in nighttime BP, but also by an increase in daytime BP (significant in the melatonin group). A nonoptimal effect for BP profile was observed in 12.5% of patients: extreme-or reverse dippers. In patients with conversion from nondippers to dippers (responders), an increase in standard deviation of normal-to-normal intervals between initial and final HRV analyses was observed. Nonresponders represented an increase in the mean circadian heart rate. To avoid nonoptimal effects, the inclusion of melatonin in pharmacotherapy of patients with CAD should be based on monitoring of circadian BP profile, before and during treatment. As melatonin caused not only a nocturnal decrease in BP but also a daytime increase, it should not be recommended in patients with 'high normal' values of BP because of the danger of induction of arterial hypertension.

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Section: Study Limitationsmentioning

confidence: 62%

Melatonin for nondippers with coronary artery disease: assessment of blood pressure profile and heart rate variability

et al. 2009

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“…Mechanisms possibly involved include a direct hypothalamic effect, a decrease in catecholamine levels, as well as relaxation of the aortic smooth muscle wall. 39,40 Similarly, in hypertensive rats, Pycnogenol dose-dependently decreased systolic blood pressure after intravenous injection. In a double-blind, placebo-controlled, crossover study in hypertensive patients, oral administration of Pycnogenol reduced slightly elevated systolic blood pressure to normal values.…”

Section: Immunohistochemical Studies For Mmp2 Bax Inos and Cox-2mentioning

confidence: 95%

Effects of Melatonin and Pycnogenol on Small Artery Structure and Function in Spontaneously Hypertensive Rats

et al. 2010

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Abstract-It was suggested that oxidative stress has a key role in the development of endothelial dysfunction, as well as microvascular structural alterations. Therefore, we have investigated 2 substances with antioxidant properties: melatonin and Pycnogenol. We treated 7 spontaneously hypertensive rats (SHRs) with melatonin and 7 with Pycnogenol for 6 weeks. We compared results obtained with those observed in 7 SHRs and 7 Wistar-Kyoto normotensive control rats kept untreated. Mesenteric small resistance arteries were dissected and mounted on a wire myograph, and a concentrationresponse curve to acetylcholine was performed. Aortic contents of metalloproteinase 2, Bax, inducible NO synthase, and cyclooxygenase 2 were evaluated, together with the aortic content of total collagen and collagen subtypes and apoptosis rate. A small reduction in systolic blood pressure was observed. A significant improvement in mesenteric small resistance artery structure and endothelial function was observed in rats treated with Pycnogenol and melatonin. Total aortic collagen content was significantly greater in untreated SHRs compared with Wistar-Kyoto control rats, whereas a full normalization was observed in treated rats. Apoptosis rate was increased in the aortas of untreated SHRs compared with Wistar-Kyoto control rats; an even more pronounced increase was observed in treated rats. Bax and metalloproteinase 2 expressions changed accordingly. Cyclooxygenase 2 and inducible NO synthase were more expressed in the aortas of untreated SHRs compared with Wistar-Kyoto control rats; this pattern was normalized by both treatments. In conclusion, our data suggest that treatment with Pycnogenol and melatonin may protect the vasculature, partly independent of blood pressure reduction, probably through their antioxidant effects. Key Words: endothelial function Ⅲ melatonin Ⅲ Pycnogenol oxidative stress R eactive oxygen species (ROS) are generated as byproducts of cellular respiration and other metabolic processes and may contribute to oxidative damage. 1,2 The ROS family includes several molecules that have divergent effects on cellular function, namely, regulation of cell growth and differentiation, modulation of extracellular matrix production and breakdown, inactivation of NO, and stimulation of protein kinases and proinflammatory genes. 3-5 Importantly, some of these actions are associated with pathological changes in cardiovascular tissues. 6 In cardiovascular disease, increased ROS production leads to endothelial dysfunction, increased vascular contractility, vascular smooth muscle cell growth and apoptosis, monocyte migration, lipid peroxidation, inflammation, and increased deposition of extracellular matrix proteins, all processes contributing to vascular damage. 7 ROS may be important in the development and maintenance of hypertension, in terms of excess production of oxidants, decreased NO bioavailability, and decreased antioxidant capacity in the vasculature and kidneys. 6,7 Hypertension may contribute to structural and functional al...

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“…It had been concluded that the hypotensive effect of melatonin in rats may be mediated by its anti-oxidative effect rather than its receptor . As reported previously, melatonin decreases plasma renin and serum norepinephrine concentrations (K-Laflamme et al, 1998). The improved NO production and decrease oxidative load after melatonin administration may lead to BP reduction (Girouard et al, 2001).…”

Section: Discussionmentioning

confidence: 64%

Protective Role of Melatonin in L-Name Induced Hypertension in Male Albino Rats

Khdhr

Mahmud

2016

SJUOZ

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Summary:The objective for the present study is to investigate the effects of melatonin (MEL) on systolic blood pressure (SBP), some biochemical parameters; serum (malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH), nitric oxide (NO)) in NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) treated rats. The male albino rats divided into five groups treated for 4 weeks: Group 1: Control rats. Group 2: L-NAME (35 mg/100 ml drinking water). Group 3: L-NAME (35 mg/100 ml drinking water) + melatonin (30 mg/Kg diet). Group 4: L-NAME (35 mg/100 ml drinking water) + melatonin (60 mg/Kg diet). Group 5: L-NAME (35 mg/100 ml drinking water) + melatonin (120 mg/Kg diet). A significant elevation in SBP and serum MDA were detected in L-NAME treated rats. Coadministration of melatonin with L-NAME prevented increasing in SBP and serum level of MDA in a dose dependent manner. On the other hand serum levels of SOD and GSH were decreased in response to L-NAME treatment, while, co-treatment with melatonin increased SOD and GSH in a dose dependent manner. The decrease serum NO level in response to L-NAME was significantly increased by melatonin but its level was decreased by increasing melatonin doses.In conclusion: L-NAME induced hypertension model was associated with decreased NO level, interestingly; melatonin increased serum NO in L-NAME treatments, but with increasing dose of MEL, NO level was decreased. Furthermore; MEL through its antioxidant properties reduced oxidative stress and prevented lipid peroxidation.

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Impaired Basal Sympathetic Tone and α1-Adrenergic Responsiveness in Association With the Hypotensive Effect of Melatonin in Spontaneously Hypertensive Rats

Cited by 89 publications

References 21 publications

Melatonin for nondippers with coronary artery disease: assessment of blood pressure profile and heart rate variability

Melatonin for nondippers with coronary artery disease: assessment of blood pressure profile and heart rate variability

Effects of Melatonin and Pycnogenol on Small Artery Structure and Function in Spontaneously Hypertensive Rats

Protective Role of Melatonin in L-Name Induced Hypertension in Male Albino Rats

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