Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1323099 (sympathomimetic)
 2,957 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clonidine (300 microgram orally) increased in man the total duration of sleep and strikingly reduced the duration of REM sleep. Yohimbine (10 mg per os) did not alter the sleep patterns in man but antagonized the effects of clonidine. These results provide evidence that an alpha sympathomimetic mechanism could suppress REM sleep and increased the total duration of sleep.
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PMID:Effect of clonidine on sleep patterns in man. 59 2

Amphetamine, a clinically used sympathomimetic central-acting drug, was administered in Spansule capsules in a blind schedule to 8 normal obse volunteers in a daily (8 a.m.) single 15 dose for 7 days. The study, conducted in the metabolic ward, included two 7 day placebo periods (pre- and post-drug). During the 1st placebo period, all subjects exhibited within the 1st 2 h of sleep a clear and significant nocturnal increase of growth hormone (GH) closely related with sleep stages 3 and 4. Thyrotropin (TSH) increase was observed between 01.00 to 04.00 h and was accompanied by a reduction of thyroxine (T4) levels. Cortisol levels presented their characteristic rhythm, clearly associated with paradoxical sleep (REM). Amphetamine significantly reduced stages 3 and 4, as well as REM sleep, and increased stage 2. GH and cortisol circadian profiles were preserved, although their magnitude was diminished. The extent of nocturnal TSH and T4 changes was significantly reduced. Drug withdrawal was accompanied by a rebound of REM sleep and a trend to recover the pretreatment TSH and T4 temporal profile. These results suggest that adrenergic neurotrasmitters may be a significant modulating system for TSH and cortisol, whereas GH nocturnal secretion may be influenced by different mechanisms.
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PMID:Neuroendocrine and electroencephalographic sleep changes due to acute amphetamine ingestion in human beings. 103 Jul 86

4-Amino-6-methoxy-1-phenyl-pyridazinium methyl sulfate (ameziniummetilsulfate, LU 1631, Regulton), in this study briefly called amezinium, was tested for possible central effects taking particular account of the mechanisms of action found for this substance in other studies. 1. The most conspicuous action of amezinium was in modifying reserpine-induced ptosis and reserpine-induced hypothermia. When amezinium is given before reserpine, the ED50 values are 0.15 and 3.9 mg/kg p.o. for both mouse and rat. These effects can be explained by a peripheral site of action since peripheral sympathomimetic effects can also be demonstrated in this dose range. Higher doses (10 mg/kg and upwards p.o.) were required to abolish reserpine-induced hypothermia 17 h after reserpine administration, an effect which probably requires a central site of action. But for imipramine, desipramine and pargyline the effective doses are the same in both experimental models (administration before and after reserpine, respectively). 2. Amezinium potentiated the effect of a threshold dose of L-dopa. Based on the central symptoms, higher doses (10 mg/kg p.o.) were also required for this effect. 3. With blood pressure increasing doses, the sleeping-waking pattern was modified in that duration and number of REM-episodes were reduced; in cats there was no parallel increase of wakefulness whilst in rats there was a slight relative increase of wakefulness. 4. Amezinium, particularly at high doses (46.4 mg/kg and upwards), exhibited a central depressant effect on the spontaneous behaviour of mice and rats and on orientational hyperactivity of mice. Based on the modification of aggregation toxicity, the effect of methamphetamine was reduced. In no dose range was there any evidence of methamphetamine-like effects (increase of motor activity, inhibition of food intake and increase of aggregation toxicity). 5. Amezinium did not affect the duration of hexobarbital anaesthesia or the coordination of mice on a rotating rod. 6. The acute toxicity of amezinium in mice and rats was low. The oral LD50 for mice was 1630 mg/kg and for rats 1410 mg/kg.
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PMID:Pharmacology of amezinium, a novel antihypotensive drug. VI. Effect on central nervous functions. 719 73

Seventeen of 67 children recovering from status asthmaticus developed sleeping bradycardia. They were compared to a control population of asthmatic children who did not develop sleeping bradycardia and differed only in the low heart rate. The authors speculate that this phenomenon is due to a combination of withdrawal of sympathomimetic stimulation and catch-up in REM (rapid eye movement) sleep.
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PMID:Sleeping bradycardia during recovery from childhood status asthmaticus. 723 16