The Pharmacology of Rauwolfia Alkaloids

Rand, M. J.; Jurevics, Helga

doi:10.1007/978-3-642-66309-3_4

Cited by 18 publications

(8 citation statements)

References 448 publications

(318 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…After reserpine treatment, the response pattern seen during tilting bears striking differences: tilting failed to increase plasma noradrenaline levels and arterial blood pressure fell during the whole manoeuvre (Figure 1). Plasma adrenaline levels were not reduced by reserpine treatment confirming the fact that the adrenal medulla is more resistant than sympathetic nerve endings to catecholamine depletion by reserpine (see Rand & Jurevics, 1977). However, during tilting, plasma adrenaline levels only increased after 5min (in contrast to control dogs) suggesting that reserpine alters the orthostatism-induced release of adrenaline from the adrenal medulla.…”

Section: Discussionmentioning

confidence: 68%

Reserpine induces vascular α₂‐adrenergic supersensitivity and platelet α₂‐adrenoceptor up‐regulation in dog

Estañ¹,

Senard²,

Tran³

et al. 1990

British J Pharmacology

View full text Add to dashboard Cite

1 The aim of the present study was to investigate the influence of catecholamine levels on the regulation of a2-adrenoceptor sensitivity in dogs 7 These results show that a 15 day treatment with reserpine induces a vascular x2-adrenergic supersensitivity and an up-regulation in platelet a2-adrenoceptors. In contrast, this phenomenon does not involve all the tissues since adipocyte a2-adrenoceptors escape the effect of reserpine. We suggest that the levels of plasma noradrenaline play an important role in the regulation of the platelet and vascular c2-adrenoceptors. In contrast, adipocyte M2-adrenoceptors are not affected by changes in plasma noradrenaline levels.

show abstract

Section: Discussionmentioning

confidence: 68%

Reserpine induces vascular α₂‐adrenergic supersensitivity and platelet α₂‐adrenoceptor up‐regulation in dog

Estañ¹,

Senard²,

Tran³

et al. 1990

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…These studies utilized the well-documented observation that monoamine oxidase, the major enzyme that degrades catecholamines, is located in the mitochondria and hence can act on cytoplasmic catecholamines but not on those stored in the synaptic vesicles (Kopin and Axelrod, 1963;Iversen, 1970). Two agents were used as controls: veratridine, which is known to induce calcium-dependent exocytosis of catecholamines (Ohta et al, 1973) and reserpine, which interferes with storage processes and causes release of catecholamine products, a large fraction of which is deaminated (Rand and Jurevics, 1977).…”

Section: Effects Of Amines On Catecholamine Deaminationmentioning

confidence: 99%

A Role for Transglutaminase in Neurotransmitter Release by Rat Brain Synaptosomes

Pastuszko

Wilson

Erecińska

1986

Journal of Neurochemistry

View full text Add to dashboard Cite

Rat brain synaptosomes exhibit calcium-dependent transglutaminase activity. This activity, measured in detergent-treated or sonicated preparations, was six- to sevenfold lower than that in the liver. The synaptosomal transglutaminase was inhibited by various amines and alpha-difluoromethylornithine, compounds known to inhibit activity of this enzyme in other tissues. The inhibitors of transglutaminase induced release of catecholamines, but not of gamma-aminobutyric acid, from synaptosomes both under basal and K+-stimulated conditions. The concentrations of the agents that caused stimulation of catecholamine release were approximately the same as those that inhibited the activity of transglutaminase. Stimulation of release was largely reduced by the withdrawal of calcium from the incubation medium. Inhibitors of transglutaminase had little effect either on the uptakes of neurotransmitters or the amounts of deaminated products of catecholamine degradation released into the medium. It is suggested that a synaptosomal transglutaminase is involved in suppressing vesicular release of catecholamines by resting (nondepolarized) neurons and that this action may also be a part of negative feedback control which prevents excessive transmitter release at the synapse during increased neuronal activity.

show abstract

“…The decrease in blood pressure elicited by intracisternal lysine-vasopressin was probably due to a decrease in sympathetic tone since it was prevented by pretreatment with guanethidine. In contrast, the oxytocin-induced hypertensive response was not modified by guanethidine, suggesting that this effect was independent of variations in sympathetic tone or could be due to adrenal medullary discharge since guanethidine has little effect on this gland (Rand & Jurevics, 1977).…”

Section: Discussionmentioning

confidence: 89%

Effects of Lysine‐vasopressin and Oxytocin on Central Cardiovascular Control

Tran

Montastruc

1982

British J Pharmacology

View full text Add to dashboard Cite

1 The cardiovascular effects of intravenous and intracisternal administration of neurohypophysial peptides were compared in dogs anaesthetized with chloralose.2 Intravenous lysine-vasopressin (0.1 to 100 mu/kg) induced a dose-dependent increase in blood pressure and a decrease in heart rate. In contrast, intracisternal lysine-vasopressin (0.01 to 10 mu/kg) induced a dose-related decrease in blood pressure and did not change heart rate. 3 Intracisternal oxytocin (1 and 10 mu/kg) increased blood pressure and did not change heart rate, whereas the same doses injected intravenously were inactive. 4 Pretreatment with guanethidine (15 mg/kg i.v. 24 h beforehand) abolished the hypotensive responses to intracisternal vasopressin but not the pressor action of intravenous vasopressin. 5 The pressor responses to central injections of oxytocin were not modified by guanethidine. 6 Hypotension elicited by intracisternal vasopressin was probably due to a decrease in sympathetic tone whereas the hypertension induced by intracisternal oxytocin was independent of variations in sympathetic tone.

show abstract

The Pharmacology of Rauwolfia Alkaloids

Cited by 18 publications

References 448 publications

Reserpine induces vascular α₂‐adrenergic supersensitivity and platelet α₂‐adrenoceptor up‐regulation in dog

Reserpine induces vascular α₂‐adrenergic supersensitivity and platelet α₂‐adrenoceptor up‐regulation in dog

A Role for Transglutaminase in Neurotransmitter Release by Rat Brain Synaptosomes

Effects of Lysine‐vasopressin and Oxytocin on Central Cardiovascular Control

Contact Info

Product

Resources

About

The Pharmacology of Rauwolfia Alkaloids

Cited by 18 publications

References 448 publications

Reserpine induces vascular α2‐adrenergic supersensitivity and platelet α2‐adrenoceptor up‐regulation in dog

Reserpine induces vascular α2‐adrenergic supersensitivity and platelet α2‐adrenoceptor up‐regulation in dog

A Role for Transglutaminase in Neurotransmitter Release by Rat Brain Synaptosomes

Effects of Lysine‐vasopressin and Oxytocin on Central Cardiovascular Control

Contact Info

Product

Resources

About

Reserpine induces vascular α₂‐adrenergic supersensitivity and platelet α₂‐adrenoceptor up‐regulation in dog

Reserpine induces vascular α₂‐adrenergic supersensitivity and platelet α₂‐adrenoceptor up‐regulation in dog