Central noradrenergic neurones and the cardiovascular actions of clonidine in the rabbit

Dollery, C. T.; Reid, John L.

doi:10.1111/j.1476-5381.1973.tb08318.x

Cited by 74 publications

(22 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is possible, however, that these excitations could be mediated by a presynaptic action of clonidine. Dollery & Reid (1973) have shown that 6-hydroxydopamine, which causes a degeneration of central catecholamine-containing neurones, greatly reduces the hypotensive response to clonidine. Since an interaction with possibly dopaminergic neurones has previously been shown to be unlikely by Bolme & Fuxe (1971), the observation of Dollery & Reid (1973) suggests that clonidine may interact at least in part with the noradrenaline-releasing neurones themselves rather than with the postsynaptic receptor.…”

Section: Resultsmentioning

confidence: 99%

“…Dollery & Reid (1973) have shown that 6-hydroxydopamine, which causes a degeneration of central catecholamine-containing neurones, greatly reduces the hypotensive response to clonidine. Since an interaction with possibly dopaminergic neurones has previously been shown to be unlikely by Bolme & Fuxe (1971), the observation of Dollery & Reid (1973) suggests that clonidine may interact at least in part with the noradrenaline-releasing neurones themselves rather than with the postsynaptic receptor. A reduction in the release of noradrenaline by sympathetic neurones in the presence of clonidine has been demonstrated by Starke, Wagner & Schumann (1972) and a reduced noradrenaline release from field-stimulated brain slices in the presence of clonidine by Farnebo & Hamberger (1971).…”

Section: Resultsmentioning

confidence: 99%

“…Thus, clonidine no longer produces hypotension after the degeneration of such neurones as a result of 6-hydroxydopamine treatment (Dollery & Reid, 1973), and the hypotension normally produced may be reduced by the use of adrenoceptor blocking agents such as phentolamine and piperoxane (Schmitt, Schmitt & Fenard, 1971). The present experiments were therefore designed to investigate the effects of clonidine directly on the central nervous system by applying the drug in the vicinity of single neurones by microiontophoresis.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

On the Mechanism of Action of Clonidine: Effects on Single Central Neurones

Anderson

Stone

1974

British J Pharmacology

View full text Add to dashboard Cite

1 Noradrenaline and clonidine were applied by microiontophoresis to single neurones in the cerebral cortex and medullary reticular formation of anaesthetized rats. 2 Of a total of 247 neurones studied, 79% of medullary units and 60% of cortical units responded in the same manner to both noradrenaline and clonidine. The usual response was a depression of neuronal firing rate. 3 It proved possible to antagonize some responses to both substances by the microiontophoresis of bulbocapnine, whilst leaving unaffected similar responses to 5-hydroxytryptamine. 4 On 13% of the cells, clonidine produced an increase of firing rate. This effect could not be attributed to a post-synaptic antagonism of tonically released endogenous noradrenaline, but may indicate a presynaptic action of clonidine, reducing noradrenaline release. 5 These observations are thought to support action on noradrenaline receptors in the brain. the idea that clonidine may have an agonist

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

On the Mechanism of Action of Clonidine: Effects on Single Central Neurones

Anderson

Stone

1974

British J Pharmacology

View full text Add to dashboard Cite

show abstract

“…The fall is preceded by a transient rise which is a peripheral effect due to vasoconstriction. But the fall is central in origin and has been obtained with minute doses of clonidine injected into the vertebral arteries (Sattler & van Zweiten, 1967;Constantine & McShane, 1968;Katic, Lavery & Lowe, 1972) into the cisterna magna (Kobinger, 1967;Kobinger & Walland, 1967; Dollery & Reid, 1973), and into the lateral or third cerebral ventricle (Schmitt, 1970). The fall is not abolished by vagotomy and is due to a decrease in sympathetic vasomotor tone.…”

Section: Introductionmentioning

confidence: 99%

Localization of the central cardiovascular action of clonidine

Bousquet¹,

Guertzenstein²

1973

British J Pharmacology

111

View full text Add to dashboard Cite

Summary The fall in arterial blood pressure with bradycardia that occurs on injection of clonidine into the cerebral ventricles and into the cisterna magna is attributed to an action on ‘chemosensitive zones’ situated at the ventral surface of the brain stem. This conclusion is based on the following results obtained in cats anaesthetized with pentobarbitone sodium. The fall in blood pressure no longer occurs on injection of clonidine (10 to 100 μg) into the cerebral ventricles when the passage of clonidine into the subarachnoid space is prevented by cannulation of the aqueduct. In this condition, the injections produce instead a rise in blood pressure. Applied bilaterally, by means of perspex rings, to the ventral surface of the brain stem, clonidine (10 μl of a 50 to 1,000 μg/ml solution placed in each ring) produces a fall in blood pressure with bradycardia, but only when the perspex rings cover the ‘chemosensitive zones’ from which changes in blood pressure and heart rate are obtained with various drugs.

show abstract

“…The therapeutic action is chiefly central (Katic, Lavery & Rowe, 1972;Dollery & Reid, 1973) although there is also evidence for a peripherally mediated reduction in plasma catecholamine concentration (Brown & Harland, 1984). Clonidine also causes short-term behavioural sedation or sleep in rabbits (Gadie, McCarthy & Tulloch, 1983), chicks and rats (Holman, Shillito & Vogt, 1971).…”

Section: Introductionmentioning

confidence: 99%

Effects of the alpha 2‐adrenergic agonist clonidine and its antagonist idazoxan on the fetal lamb.

Bamford¹,

Dawes²,

Denny³

et al. 1986

The Journal of Physiology

View full text Add to dashboard Cite

SUMMARY1. The a2-adrenergic agonist clonidine was given by aortic injection to three groups of unanaesthetized fetal lambs in utero near term. One group was intact, the second had the brain stem transacted just above the pons, and the third had bilateral section of the carotid sinus nerves and cervical vagi.2. Clonidine had similar effects in all three groups. Electrocortical activity entered a high-voltage, low-frequency episode: breathing, neck and limb movements ceased; arterial pressure remained unchanged or increased; heart rate fell or remained unchanged, and the variation in both heart rate and blood pressure was much reduced. This state lasted 10-20 min, and was followed by a period of up to 4 h during which the cycling of electrocortical activity was rapid and irregular.3. The a2-adrenergic antagonist idazoxan (0-5-2-0 mg I.A.) blocked all the actions of clonidine. When given alone it usually induced a short period of low-voltage electrocortical activity and stimulated breathing movements. These effects were present in both the intact and brain-stem-transected groups, though the stimulation of breathing was significantly reduced by brain-stem transaction. There were no consistent effects on heart rate or blood pressure.4. The effects of clonidine on fetal heart rate and electrocortical activity were similar to those described in adults, but it also had inhibitory effects, not present in adults, on fetal breathing and somatic movements.

show abstract

Central noradrenergic neurones and the cardiovascular actions of clonidine in the rabbit

Cited by 74 publications

References 35 publications

On the Mechanism of Action of Clonidine: Effects on Single Central Neurones

On the Mechanism of Action of Clonidine: Effects on Single Central Neurones

Localization of the central cardiovascular action of clonidine

Effects of the alpha 2‐adrenergic agonist clonidine and its antagonist idazoxan on the fetal lamb.

Contact Info

Product

Resources

About