Effect of Guanethidine, Hemicholinium and Mebutamate on the Hypertensive Response to Eserine and Catechol Amines

Varagić, V.M.; Vojvodić, Nikola

doi:10.1111/j.1476-5381.1962.tb01449.x

Cited by 26 publications

(4 citation statements)

References 16 publications

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“…injected at a dose of 10 mg kg −1 . Drug doses were chosen as those certain to be effective in producing in vivo blockade of β 1 ‐ and α 1 ‐adrenoceptors and sympathetic neurones, respectively (Varagić & Vojvodić, 1962; Berdeaux et al , 1977; van Meel et al , 1981).…”

Section: Methodsmentioning

confidence: 99%

Resuscitating effect of melanocortin peptides after prolonged respiratory arrest

Guarini

Bazzani

Bertolini

1997

British J Pharmacology

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1 The resuscitating activity of melanocortin peptides (MSH-ACTH peptides) was tested in an experimental model of prolonged respiratory arrest. 2 Anaesthetized, endotracheally intubated rats subjected to a 5 min period of ventilation interruption, invariably died from cardiac arrest within 6 ± 9 min of resumption of ventilation. 3 When resumption of ventilation was associated with the simultaneous intravenous (i.v.) injection of a melanocortin peptide (a-MSH or ACTH-(1 ± 24)) (160 mg kg 71) there was an almost immediate (within 1 min), impressive increase in cardiac output, heart rate, mean arterial pressure (+560% of the beforetreatment value) and pulse pressure (+356% of the before-treatment value), with full recovery of electroencephalogram after 30 ± 45 min. Blood gases and pH were normalized within 15 ± 60 min after treatment, and all treated animals eventually recovered completely and survived inde®nitely (= more than 15 days). 4 The same response was observed in adrenalectomized animals, as well as in animals pretreated with a b 1 -adrenoceptor blocking agent (atenolol, 3 mg kg 71 , i.v.), or with an a 1 -adrenoceptor blocking agent (prazosin, 0.1 mg kg 71 , i.v.), or with an adrenergic neurone blocking agent (guanethidine, 10 mg kg 71 , intraperitoneally). 5 An eect quite similar to that produced by melanocortins was obtained with ouabain (0.1 mg kg 71 , i.v.); the antioxidant drug, glutathione (75 mg kg 71 , i.v.) also produced 100% resuscitation, but the eect was slower in onset. On the other hand, adrenaline (0.005 mg kg 71 , i.v.) was able to resuscitate only 1 out of 8 rats and dobutamine (0.02 mg kg 71 , i.v.) resuscitated 4 out of 8 rats; moreover, the eect of both catecholamines was much slower in onset than that of melanocortins and the initial, impressive stimulation of cardiovascular function was absent. 6 These results show that melanocortin peptides have a resuscitating eect in a pre-terminal condition produced in rats by prolonged asphyxia. This eect seems primarily due to the restoration of cardiac function, not mediated by catecholamines. These data also suggest that these peptides may have potential therapeutic value in conditions of transient cardiac hypoxia and re-oxygenation such as occur in coronary artery disease.

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Section: Methodsmentioning

confidence: 99%

Resuscitating effect of melanocortin peptides after prolonged respiratory arrest

Guarini

Bazzani

Bertolini

1997

British J Pharmacology

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“…A large number of studies have been performed at longer intervals after the administration of a-MD (usually 16-24 hours). In the majority of these experiments, the sympathetic nerves to the spleen, heart and nictitating membranes appear to have functioned normally (STONE et al 1962;MUSCHOLL & MATTRE 1963;STONE & STAVORSKI 1963;VARMA & BENFEY 1963;SCHAEPDRYVER et ul. 1963;HAEFELY et al 1966HAEFELY et al & 1967aKADZIELAWA 1967).…”

Section: Discussionmentioning

confidence: 99%

Adrenergic Nerve Function in the Anaesthetized Rat after Treatment with α‐Methyldopa

Henning

Svensson

1968

Acta Pharmacologica et Toxicologica

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The ability of a-methyldopa (L-a-methyl-3,4-dihydroxy-phenylalanine, u-MD) to lower arterial blood pressure in animals and man is generally thought to depend on an interference with the sympathetic nervous system (reviews by SOURKES 1965;MUSCHOLL 1966;HOLTZ & PALM 1966; STONE & PORTER 1966. However, the localisation of the action of the drug within this system has not yet been established. The decrease in blood pressure may be brought about by an effect of a-MD on the central nervous system, leading to a reduced sympathetic activity, or to an effect on the peripheral adrenergic nerves, or both. The relative importance of these components is poorly understood. While there are several indications of functional impairment in the central nervous system, opinions differ as to the effect of the drug on the peripheral sympathetjc system. A number of reports indicate that a-MD may cause a moderate blockade of this system while other investigators have obtained normal responses. (For references, see reviews mentioned above and Discussion of this paper).A sympathetic blockade of importance for the antihypertensive effect of a-MD should be easily demonstrable a t the time of maximal fall in blood pressure following the administration of the drug. In a previous study (HENNING 1967) it was found that the administration of a single dose of u-M D lowered the blood pressure of conscious normotensive rats. A maximal decrease was observed 3-6 hours after the injection. In the present investigation we have carried out some tests of adrenergic nerve function on anaesthetized rats during this period, following the administration of the same dose of a-MD. The tests included lower eyelid contraction to cervical sympathetic stimulation and eyelid and blood pressure responses to injections of a ganglionic stimulant drug,

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“…These reasons also rule out the involve ment of acetylcholine release by eserine from cholinergic neurones (Carlyle, 1963;Bartolini et al, 1973). The central mechanisms which operate in the anaesthetised rats (Lesic and Varagic, 1961;Varagic and Vojvodic, 1962;Gokhale et al, 1963) would not be involved in the pithed frogs. Thus, this vasoconstrictor action of eserine, like its central excitatory ef fects (Feldberg and Hebb, 1948;Bradley et al, 1966) and nonspecific sensitizing action to various vasoconstrictors (Herron et al, 1971), appears to be a direct one and not related to its anticholinesterase activity.…”

mentioning

confidence: 99%

A Vasoconstrictor Action of Eserine Not Related to Blockade of Cholinesterase

Gambhir¹,

Pk²

1979

J Vasc Res

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Effect of Guanethidine, Hemicholinium and Mebutamate on the Hypertensive Response to Eserine and Catechol Amines

Cited by 26 publications

References 16 publications

Resuscitating effect of melanocortin peptides after prolonged respiratory arrest

Resuscitating effect of melanocortin peptides after prolonged respiratory arrest

Adrenergic Nerve Function in the Anaesthetized Rat after Treatment with α‐Methyldopa

A Vasoconstrictor Action of Eserine Not Related to Blockade of Cholinesterase

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