Inactivation of Catecholamines in the Blood Vessel Wall

Osswald, Walter

doi:10.1007/978-1-4615-9471-0_1

Central and Peripheral Mechanisms of Cardiovascular Regulation 1986

DOI: 10.1007/978-1-4615-9471-0_1

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Inactivation of Catecholamines in the Blood Vessel Wall

Walter Osswald

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1988

1992

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Cited by 3 publications

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The role of monoamine oxidase in the metabolism of exogenous noradrenaline by the human saphenous vein*

Branco¹,

Caramona²,

Araújo³

et al. 1992

Fundamemntal Clinical Pharma

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Human saphenous vein segments were obtained from patients subjected to coronary bypass surgery. As determined by HPLC-ED, the veins had a relatively low content of noradrenaline and high content of the deaminated metabolites, dihydroxyphenylglycol (DOPEG) and dihydroxymandelic acid (DOMA). In vein segments which had been incubated with 3H-noradrenaline (0.1 mumol/l), the oxidative deamination pathway predominated over the O-methylating one. Deamination occurred both at the neuronal and extraneuronal level; DOPEG appearing to be a good index of intraneuronal deamination, whereas DOMA and O-methylated and deaminated metabolites were mainly formed extraneuronally. Both MAO type A and MAO type B selective inhibitors reduced the deamination of noradrenaline; deamination was also found to be partially sensitive to semicarbazide. Inhibition of neuronal uptake or of deamination increased O-methylation. The human saphenous vein thus metabolizes exogenous noradrenaline following a pattern which substantially differs from that shown to occur in various blood vessels from other animal species.

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The role of monoamine oxidase in the metabolism of exogenous noradrenaline by the human saphenous vein*

Branco¹,

Caramona²,

Araújo³

et al. 1992

Fundamemntal Clinical Pharma

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Catecholamines: Regulation, Release and Inactivation

Nedergaard¹

1988

Pharmacology & Toxicology

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Modulation of Noradrenaline Release by Activation of Presynaptic β‐Adrenoceptors in the Cardiovascular System^a

Nedergaard

Abrahamsen

1990

Annals of the New York Academy of Sciences

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Peripheral sympathetic nerve terminals in many tissues, but not all, are endowed with beta-adrenoceptors. Activation of these result in an enhancement of noradrenaline release evoked by electrical nerve stimulation. These so-called presynaptic beta-adrenoceptors are possibly located on the outer surface of the varicosity of the noradrenergic nerves. A postsynaptic location, however, is also a possibility. The presynaptic beta-adrenoceptors appear to be of the beta 2-adrenoceptor subtype. However, specific classification is lacking. The stereospecificity of the beta-adrenoceptors is controversial. These receptors are not activated by noradrenaline released from sympathetic nerves. Adrenaline derived from the adrenal medulla may be the physiological activator. Either circulating adrenaline or adrenaline taken up by sympathetic nerve terminals and then released as a cotransmitter with noradrenaline activates the presynaptic beta-adrenoceptors. In the latter case, a "positive" feedback" loop may be formed.

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Inactivation of Catecholamines in the Blood Vessel Wall

Cited by 3 publications

References 63 publications

The role of monoamine oxidase in the metabolism of exogenous noradrenaline by the human saphenous vein*

The role of monoamine oxidase in the metabolism of exogenous noradrenaline by the human saphenous vein*

Catecholamines: Regulation, Release and Inactivation

Modulation of Noradrenaline Release by Activation of Presynaptic β‐Adrenoceptors in the Cardiovascular System^a

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About

Inactivation of Catecholamines in the Blood Vessel Wall

Cited by 3 publications

References 63 publications

The role of monoamine oxidase in the metabolism of exogenous noradrenaline by the human saphenous vein*

The role of monoamine oxidase in the metabolism of exogenous noradrenaline by the human saphenous vein*

Catecholamines: Regulation, Release and Inactivation

Modulation of Noradrenaline Release by Activation of Presynaptic β‐Adrenoceptors in the Cardiovascular Systema

Contact Info

Product

Resources

About

Modulation of Noradrenaline Release by Activation of Presynaptic β‐Adrenoceptors in the Cardiovascular System^a