Evidence for a central noradrenaline receptor stimulation by clonidine

Andén, Nils‐Erik; Corrodi, H.; Fuxé, Kjell; Hökfelt, Bernt; Hökfelt, Tomas; Rydin, Carolina; Svensson, Torgny H.

doi:10.1016/0024-3205(70)90207-9

Cited by 549 publications

(67 citation statements)

References 19 publications

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“…This suggests a direct effect of dopamine on a catecholaminergic receptor. The prior administration of haloperidol, which blocks dopamine receptors preferentially to noradrenaline receptors (Van Rossum, 1966;And~n et al, 1970;Day and Roach, 1976), failed to separate the effect of dopamine from that a-methylnoradrenaline. Also, the a-lyric drugs phentolamine and yohimbine both blocked the effect of dopamine as well as that of a-methylnoradrenaline.…”

Section: Discussionmentioning

confidence: 99%

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Effect of catecholamine-receptor stimulating agents on blood pressure after local application in the nucleus tractus solitarii of the medulla oblongata

Zandberg

Jong

Wied

1979

European Journal of Pharmacology

159

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Effect of catecholamine-receptor stimulating agents on blood pressure after local application in the nucleus tractus solitarii of the medulla oblongata, European J. Pharmacol. 55 (1979) 43--56.The effect of various catecholamines and a-mimetics, given by microinjection in the A2-region of the nucleus tractus solitarii (NTS), on blood pressure was investigated in anesthetized male rats. A dose-dependent decrease of blood pressure and heart rate was induced by adrenaline as the most effective drug, followed by noradrenaline, dopamine, a-methylnoradrenaline and octopamine. Ablation of the rostral or caudal part of the NTS, or removal of the area postrema did not diminish the effect of a-methylnoradrenaline. Higher doses of noradrenaline and a-methylnoradrenaline caused an initial rise of blood pressure, while the blood pressure lowering effect of noradrenaline was diminished, and that of a-methylnoradrenaline and dopamine delayed. Isoprenaline and the (+)-stereoisomers of noradrenaline and a-methylnoradrenaline were ineffective. The hypotensive effect of dopamine was not prevented by systemic injection of the dopamine ~-hydroxylase inhibitor FLA 63. Prior application of haloperidol, yohimbine and phentolamine antagonized the hypotensive response to dopamine and a-methylnoradrenaline. Application of peripherally effective a-mimetics into the A2-region had no or little effect, while high doses increased blood pressure. Tyramine and clonidine caused some decrease of blood pressure. Clonidine also decreased blood pressure when it was applied in the area of the locus coeruleus. Application of isoprenaline in the locus coeruleus also decreased blood pressure while in contrast adrenaline, noradrenaline, dopamine and 0l-methylnoradrenaline increased blood pressure. The present data suggest that the catecholaminergic receptors in the A2-region of the NTS differ from the classic vascular a-receptor and that the NTS also may contain structures which can antagonize the decrease in blood pressure. Catecholamines a-Mimetics Locus coeruleusDecrease of blood pressure Nucleus tractus solitarii

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Section: Discussionmentioning

confidence: 99%

“…The catecholamines, however, increased blood pressure at this site while isoprenaline decreased it. And~n et al (1970) reported that clonidine reduced noradrenaline turnover in the brain. A reduction of spontaneous firing of the noradrenaline containing neurons of the locus coeruleus has been observed following i.v.…”

Section: Discussionmentioning

confidence: 99%

Effect of catecholamine-receptor stimulating agents on blood pressure after local application in the nucleus tractus solitarii of the medulla oblongata

Zandberg

Jong

Wied

1979

European Journal of Pharmacology

159

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“…Both clonidine and xylazine may interfere with noradrenergic mechanisms presynaptically and there is also much evidence to suggest a postsynaptic mode of action for clonidine in the CNS (Haensler & Finch, 1972;Greenberg, U'Prichard & Snyder, 1976;Warnke and Hoefke, 1977). In addition it has been suggested that clonidine has inhibitory actions both on 5-HT-mediated responses in the spinal cord (Franz, Hare & Neumayr, 1978) and on 5-HT turnover (Anden, Corrodi, Fuxe, Hokfelt, Hokfelt Rydin & Svensson, 1970). Moreover, there are reports of 5-HT endings having both 5-HT and a2-receptors (Timmermans & van Zweiten, 1982); consequently it is possible that clonidine may be exerting its effects on body temperature via 5-HT neurones rather than through noradrenaline.…”

Section: Methodsmentioning

confidence: 99%

Effects of clonidine and xylazine on body temperature in the rat

Livingston¹,

Low²,

Morris³

1984

British J Pharmacology

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1Clonidine and xylazine injected intraperitoneally both produced a dose-dependent hypothermia in unanaesthetized, freely moving rats. 2 The c2-antagonist yohimbine produced an antagonism of the xylazine-induced hypothermia but a potentiation of the clonidine-induced hypothermia. 3 The opioid antagonist naloxone had little effect on the xylazine hypothermia, but potentiated the clonidine hypothermia. 4 It is concluded that whilst the two a2-agonists produce a similar hypothermic effect in the rat, they are acting by different mechanisms.

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“…Clonidine is a potent and specific agonist at a2-adrenoceptors (Starke & Altmann, 1973;Starke & Montel, 1973;Starke et al, 1974). It binds specifically to a2-adrenoceptors in the cortex (Titeler & Seeman, 1980), and as a consequence of a2-activation it reduces turnover of NA (Anden et al, 1970, Braestrup, 1974. Given systemically or by microiontophoresis, clonidine inhibits the firing of NA cells in the LC, whereas DA cells are not influenced (Svensson et al, 1975).…”

Section: Agonists and Antagonists Ofa-adrenoceptorsmentioning

confidence: 99%

Biochemical pharmacology of paradoxical sleep.

Gaillard¹

1983

Brit J Clinical Pharma

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1 The role of noradrenergic cells in the regulation of paradoxical sleep is still controversial, and experimental data have given rise to contradictory interpretations.2 Early investigations focused primarily on chemical neurotransmissions. However, the process of information transmission between cells involves many other factors, and the cell surface is an important site for transduction of messages into modifications of the activity of postsynaptic cells.3 a-adrenoceptors are believed to play an important role in the control of wakefulness and paradoxical sleep. Experimental evidence suggests that physiological modulation of receptor sensitivity, possibly by specific neuro-modulators, may be a key mechanism in synaptic transmission. 4 In the investigation of the mechanisms involved in paradoxical sleep regulation, lesions of the locus coeruleus have given equivocal results. Collateral inhibition, probably mediated by a2-adrenoceptors, appears to be a powerful mechanism. The exact temporal relationship between noradrenergic cell activation and paradoxical sleep production is not established, but 5-HT appears to be involved. Differences between paradoxical sleep and waking may be related to a physiological modulation of a2-adrenoceptor sensitivity.

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Evidence for a central noradrenaline receptor stimulation by clonidine

Cited by 549 publications

References 19 publications

Effect of catecholamine-receptor stimulating agents on blood pressure after local application in the nucleus tractus solitarii of the medulla oblongata

Effect of catecholamine-receptor stimulating agents on blood pressure after local application in the nucleus tractus solitarii of the medulla oblongata

Effects of clonidine and xylazine on body temperature in the rat

Biochemical pharmacology of paradoxical sleep.

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