Clonidine: New research in psychotropic drug pharmacology

Fielding, Stuart; Lal, Harbans

doi:10.1002/med.2610010106

Cited by 47 publications

(4 citation statements)

References 84 publications

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“…Agonists of α 2 ‐adrenoceptors produce a wide variety of effects. These include an antihypertensive action, alleviation of opiate‐withdrawal syndrome, antinociception and sedation ( Fielding & Lal, 1981 ; McDonald et al ., 1997 ). Clonidine, an agonist of α 2 ‐adrenoceptors, is extremely potent as an antinociceptive agent showing equal or greater potency than morphine in rodents ( Fielding et al ., 1978 ).…”

Section: Introductionmentioning

confidence: 99%

“…Clonidine, an agonist of α 2 ‐adrenoceptors, is extremely potent as an antinociceptive agent showing equal or greater potency than morphine in rodents ( Fielding et al ., 1978 ). Clonidine has been shown to exhibit antinociceptive activity against a wide variety of noxious stimuli such as chemical irritants, heat, pressure and electrical stimuli ( Fielding & Lal, 1981 ; Skingle et al ., 1982 ).…”

Section: Introductionmentioning

confidence: 99%

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Role of potassium channels in the antinociception induced by agonists of α₂‐adrenoceptors

Galeotti¹,

Ghelardini²,

Vinci³

et al. 1999

British J Pharmacology

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1 The e ect of the administration of pertussis toxin (PTX) as well as modulators of di erent subtypes of K + channels on the antinociception induced by clonidine and guanabenz was evaluated in the mouse hot plate test. 2 Pretreatment with pertussis toxin (0.25 mg per mouse i.c.v.) 7 days before the hot-plate test, prevented the antinociception induced by both clonidine (0.08 ± 0.2 mg kg 71 , s.c.) and guanabenz (0.1 ± 0.5 mg kg 71 , s.c.). 3 The administration of the K ATP channel openers minoxidil (10 mg per mouse, i.c.v.), pinacidil (25 mg per mouse, i.c.v.) and diazoxide (100 mg kg 71 , p.o.) potentiated the antinociception produced by clonidine and guanabenz whereas the K ATP channel blocker gliquidone (6 mg per mouse, i.c.v.) prevented the a 2 adrenoceptor agonist-induced analgesia. 4 Pretreatment with an antisense oligonucleotide (aODN) to mKv1.1, a voltage-gated K + channel, at the dose of 2.0 nmol per single i.c.v. injection, prevented the antinociception induced by both clonidine and guanabenz in comparison with degenerate oligonucleotide (dODN)-treated mice. 5 The administration of the Ca 2+ -gated K + channel blocker apamin (0.5 ± 2.0 ng per mouse, i.c.v.) never modi®ed clonidine and guanabenz analgesia. 6 At the highest e ective doses, none of the drugs used modi®ed animals' gross behaviour nor impaired motor coordination, as revealed by the rota-rod test.7 The present data demonstrate that both K ATP and mKv1.1 K + channels represent an important step in the transduction mechanism underlying central antinociception induced by activation of a 2 adrenoceptors.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of potassium channels in the antinociception induced by agonists of α₂‐adrenoceptors

Galeotti¹,

Ghelardini²,

Vinci³

et al. 1999

British J Pharmacology

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“…In addition to its effects on cardiovascular function, clonidine exerts a number of behavioural actions (Laverty & Taylor, 1969;Fielding & Lal, 1981). After injection into the ventricles or hypothalamus, clonidine has been found to increase food intake in rats (Broekkamp & van Rossum, 1972;Ritter, Wise & Stein, 1975).…”

Section: Introductionmentioning

confidence: 99%

An analysis of the effects of systemically administered clonidine on the food and water intake of rats

Sanger

1983

British J Pharmacology

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1 It is known that intracerebral injections of clonidine can induce eating in rats but it has not been clear whether systemic administration can produce similar effects. 2 Subcutaneous injections of clonidine (0.01, 0.03, 0.1 mg/kg) increased food and water intake during the 6 h period following injection in non-deprived male rats. 3 Pretreatment with a dose of yohimbine (1.0 mg/kg) shifted the clonidine dose-response curves to the right, suggesting competitive antagonism. 4 A dose of naloxone (0.1 mg/kg) produced a lowering of the clonidine dose-response curve but statistical analysis suggested that the opiate antagonist did not produce a competitive antagonism of the effect of clonidine. 5 The results are consistent with a role for M2-adrenoceptors in appetite regulation.

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“…Clo nidine, an cD-agonist which directly stimulates the pe ripheral receptors while inhibiting the CNS-mediated catecholamine release and sympathetic outflow [27][28][29], partially reversed the effects of streptozotocin. increas ing body weight gain, restoring liver glycogen content and leading to partial recovery of the pancreatic insulin in the diabetic animals.…”

Section: Discussionmentioning

confidence: 99%

Central Adrenergic Suppression Augments the Insulin and Glucagon Secretory, and the Glycogenolytic Responses in Streptozotocin-Diabetic Rats

Dunbar¹,

Colemen²,

Shaffer³

et al. 1991

Horm Res

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It has been suggested that the increased activity of the sympathetic nervous system and the resultant increase in the tissue catecholamine levels contribute to the pathogenesis of diabetes. In this study we evaluated the effect of clonidine, a central adrenergic agonist that decreases sympathetic tone, on the serum levels of glucose, insulin, glucagon and norepinephrine and on the hepatic glycogen content in normal and streptozotocin-diabetic rats. The animals were treated with clonidine 25 µg/kg/day interperitoneally for 3 weeks to suppress the central adrenergic impulses. Clonidine treatment significantly increased the weight gain, but did not affect plasma glucose, insulin, glucagon and norepinephrine in the diabetic animals. Pancreatic insulin and liver glycogen contents were significantly higher in the clonidine-treated than in the untreated diabetic rats. However, clonidine did not affect pancreatic insulin and liver glycogen content of nondiabetic animals. The intravenous administration of glucagon increased plasma glucose in the clonidine-treated, but not in the saline-treated diabetic rats. Insulin-induced hypoglycemia significantly enhanced glucagon release in clonidine-treated but not in saline-treated diabetic rats. We conclude that the suppression of central adrenergic activity may ameliorate the effects of insulin insufficiency on pancreatic hormone secretion and hepatic glycogen content.

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Clonidine: New research in psychotropic drug pharmacology

Cited by 47 publications

References 84 publications

Role of potassium channels in the antinociception induced by agonists of α₂‐adrenoceptors

Role of potassium channels in the antinociception induced by agonists of α₂‐adrenoceptors

An analysis of the effects of systemically administered clonidine on the food and water intake of rats

Central Adrenergic Suppression Augments the Insulin and Glucagon Secretory, and the Glycogenolytic Responses in Streptozotocin-Diabetic Rats

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Clonidine: New research in psychotropic drug pharmacology

Cited by 47 publications

References 84 publications

Role of potassium channels in the antinociception induced by agonists of α2‐adrenoceptors

Role of potassium channels in the antinociception induced by agonists of α2‐adrenoceptors

An analysis of the effects of systemically administered clonidine on the food and water intake of rats

Central Adrenergic Suppression Augments the Insulin and Glucagon Secretory, and the Glycogenolytic Responses in Streptozotocin-Diabetic Rats

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Role of potassium channels in the antinociception induced by agonists of α₂‐adrenoceptors

Role of potassium channels in the antinociception induced by agonists of α₂‐adrenoceptors