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)

Amphetamine is a sympathomimetic and psychotropic drug which is extensively metabolized in liver and in brain. One of its major metabolites, p-hydroxyamphetamine, is accumulated by cortical and striatal synaptosomes. In order to learn whether p-hydroxyamphetamine can be further metabolized to a catecholamine, a sensitive radioenzymatic assay was developed which couples the formation of the "catecholamphetamine" to rapid O-methylation by catechol-O-methyltransferase in the presence of [3H]-methyl-S-adenosylmethionine. Rat brain microsomes contain a cytochrome P-450-dependent monooxygenase which synthesizes catecholamphetamine from p-hydroxyamphetamine. The formation of this catechol metabolite may be involved in the development of tolerance in chronic amphetamine use.
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PMID:Formation of alpha-methyldopamine ("Catecholamphetamine") from p-hydroxyamphetamine by rat brain microsomes. 53 80

Atenolol (CAS 29122-68-7) and metoprolol (CAS 37350-58-6) are beta 1-selective adrenoceptor antagonists without intrinsic sympathomimetic activity. beta-Receptor blockers influence carbohydrate- and lipid metabolism. Liver is a central organ of these processes. The metabolic fate of a single oral atenolol and metoprolol dose and their actions on carbohydrate- and lipid parameters have been investigated. Healthy male rats received a dose reducing heart beat/min by 25% (atenolol: 6 mg/kg; metoprolol: 10 mg/kg). About 9% of atenolol is metabolized by cytochrome P-450 (P-450). P-450-dependent functions (aminopyrine-N-demethylase, hexobarbital biotransformation time) were not inhibited. Serum bilirubin was normal. Triglyceride (TG), total cholesterol and HDL-cholesterol levels of the plasma were not affected. Transient blood glucose increase was measured returning to initial value at 120 min. Metoprolol is metabolized by hepatic monooxygenases. P-450-dependent functions were inhibited correlating to the lowered P-450-content of the microsomes. High TG level and decreased HDL-cholesterol content were measured. Blood glucose was significantly high. The liposoluble metroprolol affected the hepatic functions more than the hydrophilic atenolol. The monitoring of blood glucose during beta-receptor antagonist treatment may be suggested.
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PMID:Metabolic actions of a single atenolol and metoprolol dose. 784 28

Barbiturates induce reduction of myocardial contractility and metabolism, whereas ketamine exerts a sympathomimetic effect that can mask its direct depressant effect on contractility. However, it is unclear whether barbiturates, which interfere with the cytochrome P-450 pathway, or ketamine, which inhibits nitric oxide synthesis, also alter the responsiveness of the coronary vessels to vasodilator stimuli. We hypothesized that the parameters of coronary reactive hyperemia (CRH), which reflect both the degree of myocardial metabolism and vascular reactivity, could be modified by the type of anesthesia used. In two groups of goats, anesthesia was induced either using ketamine plus nitrous oxide or pentobarbital alone. To record coronary flow an electromagnetic flow-probe was placed around the left circumflex coronary artery. In the ketamine group (n = 14) and in the pentobarbital group (n = 16) CRH was studied using the indices of myocardial metabolism and vascular dilator responsiveness. In the pentobarbital group all of the indices of myocardial metabolism were lower than in the ketamine group (i.e. the excess to debt flow ratio was 2.3+/-0.8 vs. 4.6+/-2.4; p< 0.001). Yet, some indices of vascular responsiveness (time derivative of coronary flow and the peak to basal flow ratio) were not different in the two groups. Moreover, the duration of the reactive hyperemia was shorter in the ketamine than in the pentobarbital group (118+/-47 vs. 153+/-45 s, p<0.05). It is suggested that pentobarbital decreases the indices of CRH related to metabolic activity, whereas ketamine reduces the duration of the hyperemic response, which suggests an impairment of endothelial function.
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PMID:Comparison between the effects of pentobarbital or ketamine/nitrous oxide anesthesia on metabolic and endothelial components of coronary reactive hyperemia. 1147 94