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

1. Focal extracellular recording techniques were used to study the effects of clonidine, yohimbine and tyramine on the intermittent transmitter release mechanism in the guinea-pig vas deferens in vitro. Drugs were applied locally to the varicosities located within the recording electrode. Statistical methods were used to determine whether noradrenaline (NA) acts locally to inhibit secretion from the same or a closely related release site (local regulation) on an impulse-to-impulse basis. 2. The alpha-adrenoceptor agonist, clonidine, inhibited transmitter release, an effect reversed by the alpha-adrenoceptor antagonist, yohimbine. Yohimbine alone increased action potential-evoked transmitter release, findings consistent with the idea that transmitter release is regulated through prejunctional alpha-adrenoceptors. 3. The indirectly acting sympathomimetic, tyramine, powerfully inhibited evoked transmitter release, an effect reversed by both yohimbine and phentolamine. The inhibitory effects of tyramine were greatly reduced in tissues taken from animals pretreated with reserpine. Clonidine powerfully inhibited transmitter release in reserpinized tissues showing that prejunctional alpha-adrenoceptors were functionally intact. The inhibitory effects of tyramine on transmitter release are therefore mediated indirectly through the release of endogenous NA. 4. Paradoxically, when transmitter release from a small population of variscosities on a single nerve fibre was studied in the absence of alpha-adrenoceptor antagonists, no evidence was found for local regulation of transmitter release. 5. The intermittent character of the transmitter release process makes it difficult to envisage how impulse-to-impulse regulation could occur. Furthermore, it is unlikely that NA will accumulate to any appreciable extent in the vicinity of the secreting varicosity. 6. The pharmacological evidence clearly supports the view that NA released from sympathetic nerve terminals by nerve impulses modulates subsequent transmitter release. However, the evidence does not support the view that released NA acts locally to inhibit secretion from recently activated varicosities.
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PMID:Local application of drugs to sympathetic nerve terminals: an electrophysiological analysis of the role of prejunctional alpha-adrenoceptors in the guinea-pig vas deferens. 136 24

1. Propagated Ca-spikes were recorded from isolated cervical sympathetic nerve trunks of the rat when bathed in a solution containing 5 mM Ca2+, 0.5 or 1 microM tetrodotoxin (to block Na currents) and 1 mM 4-aminopyridine (to reduce K currents). 2. Spikes persisted when external Ca2+ was replaced with Sr2+ or Ba2+, but were blocked by the addition of the following inorganic Ca-channel blockers (in descending order of potency): Cd2+ greater than La3+ greater than Ni2+ greater than Co2+ greater than Mn2+ greater than Mg2+. 3. Ca-spike amplitude was reduced by up to 90% by (-)-noradrenaline (IC50 1.5 microM). The following sympathomimetic amines imitated this effect (in descending order of potency): clonidine greater than or equal to (-)-adrenaline greater than or equal to [(-)-noradrenaline] greater than or equal to dopamine greater than (-)-phenylephrine greater than or equal to (+/-)-amidephrine. 4. Ca-spike inhibition by (-)-noradrenaline was antagonized by phentolamine (pA2 6.5). Yohimbine was about 10 times weaker than phentolamine; (+/-)-propranolol (1 microM) and prazosin (10 microM) had no clear effect. 5. (-)-Noradrenaline reduced the amplitude of the compound action potential recorded from the superior cervical sympathetic ganglion following supramaximal preganglionic trunk stimulation when recorded in normal Krebs solution and hyperpolarized the ganglion with respect to the post-ganglionic trunk. Depression of the transmitted ganglionic action potential was antagonized by phentolamine (5 microM) but not by yohimbine (1 microM); in contrast 1 microM yohimbine completely prevented the ganglionic hyperpolarization. (-)-Noradrenaline did not hyperpolarize the preganglionic cervical sympathetic nerve trunk under these recording conditions. 6. It is suggested that inhibition of transmitter release from sympathetic preganglionic fibres produced by noradrenaline results from a depression of the voltage-gated Ca current in the fibres and/or their terminals, and that this action is mediated by an alpha-adrenoceptor which does not fully conform to either alpha 1 or alpha 2 subtypes.
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PMID:Inhibition of Ca-spikes in rat preganglionic cervical sympathetic nerves by sympathomimetic amines. 253 83

1. The effect of intravenous administration of dexamphetamine [+)-Amp) on rat pupil diameter was investigated. In all experiments, the vagosympathetic trunks were sectioned bilaterally at the cervical level. 2. In rats anaesthetized with urethane, (+)-Amp (0.1-0.3 mg kg-1, i.v.) produced a dose-related increase in pupil size. The mydriatic effects of (+)-Amp were evident immediately after administration. 3. Pretreatment with the alpha 2-adrenoceptor antagonists yohimbine (1.5 mg kg-1 i.v.) or idazoxan (0.5 mg kg-1, i.v.) blocked the pupillary response to (+)-Amp. Yohimbine caused about a 30 fold shift to the right in the dose-response curve whereas idazoxan almost completely abolished the mydriatic response to (+)-Amp. 4. In contrast, pretreatment with the alpha 1-adrenoceptor antagonist phenoxybenzamine (2 mg kg-1, i.v.), failed to alter significantly the pupillary response to (+)-Amp. 5. Depletion of central nervous system (CNS) monoamines with reserpine (5 mg kg-1, i.p.) and alpha-methyl-p-tyrosine (2 x 300 mg kg-1, i.p.) prevented the pupillary response to (+)-Amp. 6. The mydriatic effect of (+)-Amp was present only in preparations that had intact parasympathetic neural tone to the iris. Central preganglionic denervation of the oculomotor nerve abolished the mydriatic response of (+)-Amp. 7. These results indicate the (+)-Amp acts in the CNS to produce mydriasis in the anaesthetized rat by stimulating CNS postsynaptic alpha 2-adrenoceptors, findings that are consistent with the hypothesis that (+)-Amp acts predominantly as an indirect sympathomimetic agent to release endogenous stores of a monoaminergic neurotransmitter (perhaps noradrenaline).
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PMID:Mechanism of dexamphetamine-induced mydriasis in the anaesthetized rat. 256 90

Yohimbine is an alkaloid obtained from the Corynanthe yohimbe tree and other biological sources. Yohimbine is currently approved in the United States for erectile dysfunction and has undergone resurgence in street use as an aphrodisiac and mild hallucinogen. In recent years yohimbine use has become common in body-building communities for its presumed lipolytic and sympathomimetic effects. We describe a 37-year-old bodybuilder in which severe acute neurotoxic effects occurred in 2 h after yohimbine ingestion. The patient presented with malaise, vomiting, loss of consciousness, and repeated seizures after ingestion of 5 g of yohimbine during a body-building competition in a gymnasium. His Glasgow Coma Score was 3, requiring orotracheal intubation. Two hours after admission, vital signs were blood pressure 259/107 mmHg and heart rate 140 beats/min. Treatment with furosemide, labetalol, clonidine, and urapidil and gastrointestinal decontamination were performed. Twelve hours later the patient was extubated with normal hemodynamic parameters and neurological examination. The yohimbine blood levels at 3, 6, 14, and 22 h after ingestion were 5,240; 2,250; 1,530; and 865 ng/mL, respectively, with a mean half-life of 2 h. Few data are available about yohimbine toxicity and the related blood levels. This is a case of a large ingestion of yohimbine in which severe hemodynamic and neurological manifestations occurred and elevated blood levels of yohimbine were detected.
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PMID:Acute neurotoxicity after yohimbine ingestion by a body builder. 1964 Feb 35