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J Roquebert

Publications and source records attributed to J Roquebert.

9 recordsLinked to original sources
PubMed1992

Effects of quinpirole on autonomic nervous control of heart rate in rats.

The effects of quinpirole, a specific dopamine DA2 receptor agonist, on autonomic nervous control of heart rate, were studied in normotensive pithed rats, by analysing its action on the tachycardia and bradycardia evoked by electrical stimulation of the cardioaccelerator (10 V; 1 ms; 0.5, 1, 3, 6 Hz) and vagus (10 V; 1 ms; 3, 6, 9 Hz) nerves respectively. Quinpirole (10-50-100 micrograms kg-1 iv) reduced the cardioacceleration elicited by electrical stimulation but not that by noradrenaline (3 micrograms kg-1 iv). The effect on electrical stimulation was blocked by domperidone (0.5 mg kg-1 iv) but not by SCH 23390 (0.2 mg kg-1 iv) or idazoxan (0.3 mg kg-1 iv). At 1, 5, 10, 30 micrograms kg-1 iv, quinpirole decreased vagal but not acetylcholine-induced bradycardia. The effect on electrical stimulation was inhibited by domperidone (0.5 mg kg-1 iv) but not by SCH 23390 (0.2 mg kg-1 iv), prazosin (0.1 mg kg-1 iv) or idazoxan (0.3 mg kg-1 iv). The data point to the presence of presynaptic and/or ganglionic dopamine receptors in the sympathetic and parasympathetic innervation of the rat heart, where stimulation inhibits the release of neuromediators.

Animals↗
PubMed1992

Effect of quinpirole on neurogenic vasoconstriction in the in situ autoperfused hindquarters and renal vascular beds of the rat.

1. The effects of local administration of quinpirole were studied in the in situ autoperfused hindquarters and renal vascular beds, in order to assess whether presynaptic dopamine receptors in these vascular systems could play a role in the hypotensive effect of this agonist. 2. In both preparations, local injection of quinpirole did not alter perfusion pressure, but reduced the pressor response to electrical stimulation of the sympathetic innervation. Increases in perfusion induced by local administration of noradrenaline were not altered by quinpirole. 3. The inhibitory effect of quinpirole on the stimulation-evoked pressor responses was completely antagonized by intravenous administration of the DA2-receptor antagonist domperidone (0.5 mg kg-1) but not by the DA1-receptor antagonist SCH 23390 (0.3 mg kg-1) or the alpha 2-adrenoceptor antagonist idazoxan (0.3 mg kg-1). 4. The results indicate that quinpirole inhibits neurally induced pressor responses in the autoperfused hindquarters and renal vascular beds of the rat by stimulation of presynaptic dopamine receptors. These receptors may be involved in the hypotensive action of quinpirole in the rat.

Adrenergic alpha-Antagonists↗
PubMed1991

Pharmacological characterization of dopamine receptors in parasympathetic innervation of rat heart.

The action of dopamine agonists (apomorphine, bromocriptine, pergolide and quinpirole) on the bradycardia induced in vivo by electrical stimulation of the vagus nerves was studied in pithed rats pretreated with atenolol. The dopamine agonists decreased significantly the vagal-induced but not the acetylcholine-induced bradycardia. The first effect was blocked by (S)-sulpiride or domperidone but not by yohimbine, prazosin or SCH 23390. Both effects were antagonized by methylatropine. The data suggest the presence of presynaptic and/or ganglionic dopamine DA2 receptors in the parasympathetic innervation of the rat heart, stimulation of which inhibits the release of acetylcholine.

Acetylcholine↗
PubMed1990

Effect of bromocriptine on neurogenic vasoconstriction in the isolated autoperfused hindquarters of the rat.

The effects of local administration of bromocriptine were studied in the isolated autoperfused hindquarters of the rat, and compared to the actions of apomorphine and pergolide. Local injection of bromocriptine (1 microgram kg-1) (into the hindquarters) did not alter perfusion pressure, but reduced the pressor response to electrical stimulation of the lumbar sympathetic chains at all frequencies used (0.5-10 Hz; 5 ms; 35 V). Bromocriptine (1 microgram kg-1) did not alter the increases in perfusion pressure induced by local administration of noradrenaline. The effects of local administration of apomorphine (1 microgram kg-1) and pergolide (1 microgram kg-1) were similar to that of bromocriptine. The inhibitory effect by bromocriptine, apomorphine and pergolide of the stimulation-evoked pressor responses was completely antagonized by intravenous administration of the dopamine receptor antagonist sulpiride (0.3 mg kg-1) but was not by the alpha 2-adrenoceptor antagonist yohimbine (1 mg kg-1). In this dose, yohimbine antagonized the inhibitory effect of the alpha-adrenoceptor agonist clonidine (1 microgram kg-1). The inhibitory effect of clonidine was not altered by sulpiride but was antagonized by yohimbine. The results indicate that bromocriptine like apomorphine and pergolide inhibit neurally-induced pressor responses in the autoperfused hindquarters of the rat by stimulation of presynaptic dopamine receptors. Stimulation of these receptors leading to a fall in noradrenaline release and consequently of vasomotor tone, might at least in part explain the vasodilatator effects of bromocriptine in the rat.

Animals↗
PubMed1990

Cardiovascular effects of bromocriptine in rats: role of peripheral adrenergic and dopaminergic receptors.

1. Experiments were designed to study the involvement of alpha-adrenoceptors and dopamine receptors in the hypotensive and bradycardic actions of bromocriptine in rats. 2. Intravenous administration of bromocriptine reduced blood pressure and heart rate which was inhibited by ganglionic blocking agents or by pithing. 3. The fall in blood pressure produced by bromocriptine was not modified by atropine, atenolol, prazosin, yohimbine, bilateral vagotomy or carotid ligation, but was blocked by sulpiride, domperidone and haloperidol. 4. The bradycardia produced by bromocriptine in intact rats was assumed to be mediated by the autonomic nervous system since it was partly reduced by bilateral vagotomy or atenolol, and entirely prevented by pithing. Furthermore, sulpiride but not yohimbine antagonized this effect. 5. In pithed rats, bromocriptine decreased both the pressor response (above 10 micrograms kg-1) and the tachycardia (above 50 micrograms kg-1) elicited by electrical stimulation of spinal cord outflow. Both effects were inhibited by sulpiride or yohimbine. 6. In pithed rats, bromocriptine did not affect the hypertension due to exogenous noradrenaline, phenylephrine, B-HT 920, nor the bradycardia evoked by stimulation of the cardiac muscarinic receptors by carbachol. 7. These results suggest that, in rats, bromocriptine produces hypotension via an action on presynaptic and/or ganglionic dopamine receptors, and causes bradycardia by activation of central dopamine receptors.

Anesthesia↗