- Oct 2018
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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SWS was generally not affected. It is concluded that beta 1 neurotransmission is directly involved in the regulation of PS.
Full text summary: Beta 1 but not beta 2 is involved in REM sleep generation. High dose propranolol (which is not selective) practically obliterated REM sleep. Selective beta 1 agonism restored REM, while selective beta 2 agonism did not.
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- Aug 2018
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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In these two systems, the alpha 1 adrenergic receptor reappearance followed a monoexponential kinetic allowing to determine the half-life of the receptor (23h in vitro, 33h in vivo) as well as the rate of receptor synthesis and degradation.
Thus, the effective pharmacological half life of phenoxybenzamine is roughly 1 day.
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www.ncbi.nlm.nih.gov www.ncbi.nlm.nih.gov
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Although atenolol had no effect on subjective measures of sleep this hydrophilic drug also reduced REM frequency, suggesting that either it has some central effect, or that REM reduction is due to a peripheral 'shielding' effect.
Alternatively, it could have been nocturnal hypotension that was causing the sleep disruption.
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Analysis of the subjective questionnaires showed that recollection of dreaming and awakening in the night was increased by the three lipophilic drugs, propranolol, metoprolol, and pindolol. These results confirm reports in the literature but are contrary to those expected from considering the effects of noradrenaline on sleep. Analysis of physiological records confirmed subjects' reports that waking was increased by the lipophilic drugs. Dreaming (rapid eye movement sleep, REM) was reduced, as predicted from knowledge of the effect of noradrenaline on sleep. Increased awakening leads to an increase in remembered dreaming which explains the otherwise paradoxical results.
Surprisingly, beta-blockers, unlike alpha-blockers, appear to impair sleep.
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These results confirm reports in the literature but are contrary to those expected from considering the effects of noradrenaline on sleep. Analysis of physiological records confirmed subjects' reports that waking was increased by the lipophilic drugs. Dreaming (rapid eye movement sleep, REM) was reduced, as predicted from knowledge of the effect of noradrenaline on sleep. Increased awakening leads to an increase in remembered dreaming which explains the otherwise paradoxical results.
Surprisingly, beta-blockers, unlike alpha-blockers, appear detrimental to sleep. I would speculate that this could be the result of a shift in autonomic tone, similar to how caffeine tends to lower heart rate.
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- Oct 2017
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www.lifeextension.com www.lifeextension.com
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Beta blockers have long been associated with sleep disturbances such as difficulty falling asleep, staying asleep, and insomnia. They have been shown to reduce the production of melatonin via specific inhibition of beta-1 adrenergic receptors. Melatonin is a hormone secreted by the pineal gland in the brain, and helps in maintaining normal circadian rhythms.6,20-21 People with hypertension already have a lower melatonin production rate than those with normal blood pressure.22
The question becomes, then, do beta blockers impair sleep when exogenous melatonin is administered concurrently?
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