Biological Activity of 3-Methoxy-Catecholamines

Champagne, Jacques; D'Iorio, A.; Beaulnes, A.

doi:10.1126/science.132.3424.419

Cited by 14 publications

(3 citation statements)

References 6 publications

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“…These results clearly suggest a 3-adrenoceptor antagonistic property of these 0methylated CA. We could not confirm findings in rabbit aortic strips (14,56) or in whole guinea pig atria (44), which suggested weak adrenergic agonistic potency of MN and NMN. We recommend reevaluation these studies since the observed small effects of MN and NMN might have arisen from the contamination with free CA or from noradrenergic innervation of these tissues.…”

Section: Discussioncontrasting

confidence: 61%

Restricted Alpha- and Beta-Adrenoceptor Affinity of Sulfoconjugated Catecholamines in Human Mononuclear Leukocytes, Platelets, and Fat Cells and Reduction of the Postreceptor Mechanisms

Werle

Michel²,

Lenz³

et al. 1988

Int J Sports Med

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Section: Discussioncontrasting

confidence: 61%

Restricted Alpha- and Beta-Adrenoceptor Affinity of Sulfoconjugated Catecholamines in Human Mononuclear Leukocytes, Platelets, and Fat Cells and Reduction of the Postreceptor Mechanisms

Werle

Michel²,

Lenz³

et al. 1988

Int J Sports Med

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“…Both drugs show unexpected effects in the nictitating membrane as tolazoline is a competitive a-receptor blocking agent in most tissues (Goodman & Gilman, 1975) Beaulnes, 1960;Pruss, Maengwyn-Davies & Wurzel, 1965). If the presynaptic a-adrenoceptors of the nictitating membrane were identical with the postsynaptic a'adrenoceptors then both tolazoline and metanephrine would be expected to decrease 3H-transmitter release elicited by nerve stimulation in the range of concentrations in which they stimulate the postsynaptic a-receptors.…”

Section: Discussionmentioning

confidence: 99%

Differences Between Presynaptic and Postsynaptic Α‐adrenoceptors in the Isolated Nictitating Membrane of the Cat: Effects of Metanephrine and Tolazoline

Arbilla¹,

Langer²

1978

British J Pharmacology

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1 The a-adrenoceptor blocking agent, tolazoline, and the O-methylated metabolite of adrenaline, metanephrine, produced a concentration-dependent increase of tension in the smooth muscle of the cat isolated nictitating membrane. These effects were considered to be due to the activation of postsynaptic a-adrenoceptors. 2 The responses to nerve stimulation of this muscle were neither potentiated nor blocked by tolazoline (0.1 to 10 jiM) or metanephrine (1 to 10 gM).3 3H-transmitter overflow evoked by electrical stimulation was not modified by tolazoline or metanephrine in concentrations in which these drugs stimulated the postsynaptic a-adrenoceptors. 4 Since tolazoline and metanephrine failed to activate the presynaptic a-adrenoceptors of the cat nictitating membrane under experimental conditions in which they stimulated the postsynaptic a-adrenoceptors, these results further support the view that the presynaptic (@2) adrenoceptors differ from the postsynaptic (a,) adrenoceptors.

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“…Normetanephrine is active at adrenergic receptor sites although it is far weaker than norepinephrine (7). It therefore can probably act as an antagonist to norepinephrine.…”

Section: Discussionmentioning

confidence: 99%

The Metabolism of Norepinephrine in Depressions: Differences and Effects of Therapies

Rosenblatt

Chanley

1966

Canadian Psychiatric Association Journal

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The metabolism of infused H3-norepinephrine was studied in twenty psychiatric patients with depression. A difference was found in the metabolism in those patients classified as manic-depressive in that they tended to have a definite increase in the urine in the proportion of those metabolites which retain the amine group as compared to the metabolites which had undergone oxidative deamination (N/O ratio). The main amine metabolite was normetanephrine while the main oxidized metabolite was vanillomandelic acid. Patients diagnosed as reactive depression also tended to have an elevated N/O ratio, but to a lesser degree than the manic-depressives. Those patients with involutional psychosis or schizophrenia with depression did not differ from the normals in the amine metabolism. E.C.T. appears to be especially effective in those patients with an abnormal amine pattern and it also corrects the disturbance in the metabolism. Chlorpromazine, imipramine, amitriptyline and chlordiazepoxide cause a marked change in the metabolic pattern of norepinephrine. Evidence is cited which suggests that the altered norepinephrine metabolism may result in an elevation of normetanephrine at synaptic sites which could antagonize the action of sympathetically-released norepinephrine.

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Biological Activity of 3-Methoxy-Catecholamines

Cited by 14 publications

References 6 publications

Restricted Alpha- and Beta-Adrenoceptor Affinity of Sulfoconjugated Catecholamines in Human Mononuclear Leukocytes, Platelets, and Fat Cells and Reduction of the Postreceptor Mechanisms

Restricted Alpha- and Beta-Adrenoceptor Affinity of Sulfoconjugated Catecholamines in Human Mononuclear Leukocytes, Platelets, and Fat Cells and Reduction of the Postreceptor Mechanisms

Differences Between Presynaptic and Postsynaptic Α‐adrenoceptors in the Isolated Nictitating Membrane of the Cat: Effects of Metanephrine and Tolazoline

The Metabolism of Norepinephrine in Depressions: Differences and Effects of Therapies

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