Antihypertensive Effects of Alpha‐methylated Catecholamine Analogues in the Rat*

Brunner, H.; Hedwall, P. R.; Maître, L.; Meier, M.

doi:10.1111/j.1476-5381.1967.tb02117.x

Cited by 20 publications

(3 citation statements)

References 32 publications

(30 reference statements)

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“…Following the administration of a-methyl-DA or a-methyl-NA, peripheral stores of NA are depleted at least as much as after a-MD. Yet, the two a-methylated amines lack antihypertensive properties in the rat (BRUNNER et al 1966(BRUNNER et al & 1967HENNING 1967). It would appear that the theory of false transmission, in its simplest outline, does not adequately explain the mode of action of a-MD.…”

Section: Discussionmentioning

confidence: 99%

Interaction of DOPA Decarboxylase Inhibitors with the Effect of α‐Methyldopa on Blood Pressure and Tissue Monoamines in Rats¹

Henning

1969

Acta Pharmacologica et Toxicologica

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Several attempts have been made to explain the antihypertensive properties of a-methyldopa (a-MD) and the effects of this drug on monoamine metabolism. It is well known that a-MD can be metabolized in vivo to form a-methyldopamine (a-methyl-DA) and a-methylnoradrenaline (amethyl-NA) (CARLSSON & LINDQVIST 1962; MUSCHOLL & MA~TRE 1963 ; SCHUMANN & GROBECKER 1964; TORCHIANA et al. 1964; PORTER et af. 1965).DAY & RAND (1964) obtained a moderate reduction of the response to stimulation of the peripheral sympathetic nerves after a-MD and found a-methyl-NA to be a weaker vasoconstrictor than NA. The suggestion was made that a-methyl-NA formed from a-MD may serve as a "false transmitter" in place of NA in the sympathetic nerves; the effectiveness of sympathetic impulses would then be diminished, this leading to a reduction in blood pressure.A prerequisite of this hypothesis is that the prevention of the synthesis of the false transmitter from a-MD should abolish the hypotensive action. Only few studies seem to have been performed to determine the validity of this implication. SJOERDSMA et al. (1963) reported that an inhibitor of DOPA decarboxylase, a-hydrazino-a-methyl-P-(3,4-dihy-droxypheny1)-propionic acid (MK 485) was unable to counteract the hypotensive effect of a-MD in man. However, DAVIS et al. (1963) found that in the rat the decarboxylase inhibitor N-2-hydroxybenzyl-N-methylhydrazine (NSD 1039) antagonized this effect. 'These results were presented in a preliminary form at the joint meeting of the British and Scandinavian Pharmacological Societies, Edinburgh, July 9th-I Ith, 1968 (HENNINC 1968).

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Section: Discussionmentioning

confidence: 99%

Interaction of DOPA Decarboxylase Inhibitors with the Effect of α‐Methyldopa on Blood Pressure and Tissue Monoamines in Rats¹

Henning

1969

Acta Pharmacologica et Toxicologica

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“…MAiTRE [129] found no antagonism of norepinephrine-induced hypertension by IX-methylnorepinephrine in peripheral organs, nor could a correlation between catecholamine depletion in the heart and pressor response be established [130]. A third hypothesis has, therefore, advanced postulating a central IX-receptor blockade [131].…”

Section: ~H2mentioning

confidence: 97%

Antihypertensive Agents

Wilhelm¹,

deStevens²

1976

Progress in Drug Research/Fortschritte Der Arzneimittelforschung/Progrés Des Recherches Pharmaceutiques

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“…This compound also can replace norepinephrine in the storage granules where it is released by nervous stimulation (BRUNNER et al, 1967). This compound also can replace norepinephrine in the storage granules where it is released by nervous stimulation (BRUNNER et al, 1967).…”

Section: Adrenergic Neuron Blocking Agentsmentioning

confidence: 99%

Concepts in Biochemical Pharmacology

Brodie¹,

Gillette²,

Ackerman³

1975

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This work is subject to copyright. All rights are reserved, whether the whole or part of the material is concerned specifically those of translation, reprinting, re-use of illustrations, broadcasting, reproduction by photocopying machine or similar means, and storage in data banks. Under § 54 of the German Copyright Law where copies are made for other than private use, a fee is payable to the publlsher, the amount of the fee to be determined by agreement with the publisher. © by Springer-Verlag Berlin· Heidelberg 1975. Softcover reprint of the hardcover ist edition 1975 Library of Congress Cataloging in Publication Data (Revised) Main entry under title: Concepts in biochemical pharmacology. Handbuch der experlmentellen Pharmakologie. Handbook of experimental pharmacology. New series, v. XXVIII, 1, etc. Includes bibliographies. I. Drug metabolism-Collected works.!. Argy, W. P. II. Brodie, B. B., ed. III. Gillette, James R., 1928-ed. IV. Ackerman, Helen S., ed. V. Series: Handbuch der experimentellen Pharmakologle, v. XXVIII, 1 QP905.H3 Bd. 28, t. 1, etc. [RM301] 615'. 7 79-135957 ISBN 0-387-05134-1. The use of general descriptive names, trade names, trade marks, etc. in this pUblication, even if the former are not especially Identified, is not to be taken as a sign that such names, as understood by the Trade Marks and Merchandise Marks Act, may accordlngiy be used freely by anyone. PrefacePart 3 of the Handbook of Experimental Pharmacology (Concepts in Biochemical Pharmacology) applies the principles enunciated in Parts 1 and 2 to clinical pharmacology and toxicology. The major objective is to elucidate the many factors that determine the relationships between pharmacokinetic aspects of the disposition and metabolism of drugs and their therapeutic or toxic actions in man.Because of the more restricted information obtainable in human studies, this volume reflects the editors' bias that an understanding of pharmacokinetics is fundamental for assessing pharmacologic or toxicologic effects of drugs in humans. The first chapter is a unique primer on when to apply and how to use pharmacokinetic tools in human pharmacology. The second chapter explains the general assumptions underlying pharmacokinetic approaches both in simple terms for the novice and in mathematical form for the more sophisticated reader.Several chapters on determinants of drug concentration and activity discuss drug absorption, drug latentiation, drugs acting through metabolites, enterohepatic drug circulation, influence of route of drug administration on response, genetic variations in drug disposition and response, age differences in absorption, distribution and excretion of drugs, and pathologic and physiologic factors affecting absorption, distribution and excretion of drugs and drug response. The focus of these chapters is data obtained in human, rather than animal, studies. Most of the chapters contain new material never summarized previously.The section on drug interactions opens with a chapter in which all drug interactions are viewed as result...

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Antihypertensive Effects of Alpha‐methylated Catecholamine Analogues in the Rat*

Cited by 20 publications

References 32 publications

Interaction of DOPA Decarboxylase Inhibitors with the Effect of α‐Methyldopa on Blood Pressure and Tissue Monoamines in Rats¹

Interaction of DOPA Decarboxylase Inhibitors with the Effect of α‐Methyldopa on Blood Pressure and Tissue Monoamines in Rats¹

Antihypertensive Agents

Concepts in Biochemical Pharmacology

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Antihypertensive Effects of Alpha‐methylated Catecholamine Analogues in the Rat*

Cited by 20 publications

References 32 publications

Interaction of DOPA Decarboxylase Inhibitors with the Effect of α‐Methyldopa on Blood Pressure and Tissue Monoamines in Rats1

Interaction of DOPA Decarboxylase Inhibitors with the Effect of α‐Methyldopa on Blood Pressure and Tissue Monoamines in Rats1

Antihypertensive Agents

Concepts in Biochemical Pharmacology

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Interaction of DOPA Decarboxylase Inhibitors with the Effect of α‐Methyldopa on Blood Pressure and Tissue Monoamines in Rats¹

Interaction of DOPA Decarboxylase Inhibitors with the Effect of α‐Methyldopa on Blood Pressure and Tissue Monoamines in Rats¹