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

1 When cat spleen slices were exposed to a potassium-enriched (140 mM) Krebs solution, 367 +/- 31 ng g-1 5 min-1 of noradrenaline (NA) was released into the bathing medium. 2 Phenylephrine and clonidine (10(-7) to 10(-3) M) did not significantly modify the potassium-evoked NA release; acetylcholine decreased it in a dose-dependent manner. 3 Phenoxybenzamine increased NA release by 50% but phentolamine did not alter it; high concentrations of this drug greatly decreased NA release. Cocaine increased the NA release by about 30%. 4 It is suggested that the failure of sympathomimetic amines to depress, and of alpha-adrenoceptor blocking agents to enhance the release of NA by high potassium concentrations may be related to prolonged depolarization of the nerve terminals, which may desensitize presynaptic alpha-receptors. The fact that the same drugs are able to modify NA release during electrical nerve stimulation may be ascribed to the much shorter periods of depolarization occurring under these conditions.
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PMID:Release of noradrenaline from cat spleen slices by potassium. 2 81

Haemorrhagic shock was produced in anaesthetized dogs by bleeding into a blood reservoir system. The blood level of the reservoir was adjusted at a level above the heart, corresponding to a mean arterial blood pressure of 6.7 kPa (50 mm Hg). The dogs were treated with hydrocortisone and the adrenergic alpha-receptor blocking agent phenoxybenzamine during the hypotension period. Hydrocortisone (80-160 mg kg-1) was found to induce vasodilation, which, however, was of a very small magnitude and was of short duration. Phenoxybenzamine given after hydrocortisone caused very pronounced vasodilation. Hydrocortisone (80 mg kg-1) given after phenoxybenzamine also showed a vasodilator activity, which seemed to be greater than that of the same dose of hydrocortisone given alone. Thus, the vasodilator action of hydrocortisone does not seem to be due to an alpha-receptor blockade of the drug. The vasodilator action of phenoxybenzamine given after hydrocortisone was greater than that of even higher doses of the drug given alone. From the present findings and the fact that corticosteroids are known to potentiate the sympathomimetic action of catecholamines, it is suggested that the hydrocortisone-induced potentiation of the vasodilation action of phenoxybenzamine found is related to an increased vascular adrenergic beta-receptor tone.
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PMID:Haemodynamic effects of massive doses of hydrocortisone and the interaction with phenoxybenzamine in controlled haemorrhagic shock in the dog. 99 47

1. Using field stimulation with short trains of pulses (< 10 per train), the post-ganglionic motor transmission in the mammalian vas deferens has been further analysed pharmacologically.2. In preparations taken from guinea-pigs, rats and rabbits the effects of the indirectly sympathomimetic drugs, tyramine and cocaine, could be explained entirely on the basis of the actions of released, endogenous noradrenaline.3. Tyramine produced a contraction in vasa taken from normal rats but not from normal guinea-pigs. The tyramine contraction was due to release of endogenous noradrenaline because it was not seen in preparations taken from reserpinized rats and because it was abolished in normal vasa by phenoxybenzamine or phentolamine, thus denying the supposed inaccessibility, to alpha-blockers, of the motor alpha-adrenoceptors activated by endogenous noradrenaline.4. Phenoxybenzamine or phentolamine failed to block post-ganglionic motor transmission in rat and in guinea-pig vasa.5. Tyramine strongly inhibited motor transmission in vasa taken from normal but not from reserpinized guinea-pigs.6. Tyramine produced inhibition of motor transmission in phenoxybenzamine-treated preparations taken from normal but not from reserpinized rats.7. Cocaine inhibited motor transmission in guinea-pig and in rat vasa. This effect was not due to a local anaesthetic or to a smooth-muscle depressant action because it did not occur in preparations taken from reserpinized animals.8. The inhibitory effect of tyramine or cocaine was not abolished by beta-adrenoceptor blockade with propranolol.9. Whereas reserpinization abolished the tyramine- and cocaine-inhibitions, it did not affect the inhibitory actions of noradrenaline or of PGE(2).10. Indomethacin and sodium meclofenamate, which suppress prostaglandin synthesis, did not affect the twitch-inhibiting actions of noradrenaline, tyramine or cocaine.11. These results provide further support for the conclusion that post-ganglionic motor transmission to the vas deferens is non-adrenergic in these species and assign to endogenously released noradrenaline an inhibitory role upon motor transmission.
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PMID:Inhibition of post-ganglionic motor transmission in vas deferens by indirectly acting sympathomimetic drugs. 434 26

1. The mechanism by which sympathomimetic and certain other amines enhance blockade of the alpha-adrenoceptors by the non-equilibrium antagonist N-ethoxycarbonyl-2-ethoxy-1,2-dihydroquinoline (EEDQ) in strips of rabbit aorta was examined.2. Non-equilibrium blockade of the 5-hydroxytryptamine receptors by EEDQ was not increased by sympathomimetic amines and was decreased by 5-hydroxytryptamine.3. Low concentrations of reversible competitive antagonists appeared to protect selectively against the additional blockade by EEDQ which develops in the presence of an amine.4. Phenoxybenzamine potentiated EEDQ blockade of the alpha-receptors but not of the 5-hydroxytryptamine receptors.5. Augmentation of EEDQ blockade was also detected in a variety of other tissues, but not in segments of rabbit intestine where alpha-adrenoceptors mediate an inhibitory response.6. It was concluded that EEDQ acts at two sites in antagonizing alpha-receptor mediated responses, and that one of these sites (site II) is separate from the site of action of agonists and phenoxybenzamine (site I). Amines which enhance blockade appear to exert their action by combining with a third site (site III), which may induce a conformational alteration at site II.7. It appears that the alpha-adrenoceptor may have multiple sites for drug interaction.
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PMID:Mechanism of potentiation by amines of non-equilibrium blockade of the alpha-adrenoceptor. 472 49

1--The influence of substituted 1-phenyl-2-amino-ethan-1-ols on prostaglandin and thromboxane biosynthesis was studied using ram seminal vesicle microsomes and homogenates of rat lung and of rat stomach fundus. 2--Clear structure-activity relationships were to be seen regarding the effects of sympathomimetic drugs on prostacyclin (PGI2) biosynthesis in the rat stomach fundus homogenates. 3'- and 4'-Monohydroxy-phenyl derivatives as well as 3',4'-dihydroxy-phenyl derivatives stimulated prostaglandin and thromboxane B2 (TXB2) biosynthesis. Contrary to this the 3',5'-dihydroxy-phenyl derivatives orciprenaline, terbutaline and fenoterol were inhibitors of the biosynthesis in rat organ homogenates. 3--All the sympathomimetic drugs tested stimulated cyclo-oxygenase. Orciprenaline suppressed the adrenaline-activated cyclo-oxygenase in a dose-dependent manner. 4--The effects of adrenoceptor antagonists were also studied. Phenoxybenzamine had little effect on cyclo-oxygenase activity whereas phentolamine markedly increased the rate of oxygen uptake. Both the (+)- and (-)-optical isomers of propranolol had no effect on either basal or adrenaline-stimulated oxygen uptake. In contrast, the (+)- and (-)-isomers of pindolol inhibited basal and adrenaline-stimulated uptake.
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PMID:Influence of sympathomimetic drugs (1-phenyl-2-amino-ethan-1-ol derivatives) on the biosynthesis of prostaglandins and thromboxane B2. 640 94