THE NEUROBIOLOGICAL IMPLICATIONS OF CLONIDINE HCl

Gold, Mark S.; Pottash, A. Carter

doi:10.1111/j.1749-6632.1981.tb12809.x

Cited by 36 publications

(21 citation statements)

References 46 publications

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“…Recent research has suggested that there may be interactions between opioid and x-adrenergic mechanisms in the central nervous system and clonidine has been used clinically to treat withdrawal from opiates (Gold & Pottash, 1981). It has also been proposed that adrenergic and opioid systems may interact in the central control of appetite (Morley, 1980).…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…This view is supported by evidence that clonidine attenuates symptoms associated with short-term opiate (Gold & Pottash, 1981), alcohol (Björkqvist, 1975), and nicotine (Glassman, Jackson, Walsh, Roose, & Rosenfeld, 1984) withdrawal in humans. For example, clonidine decreases craving, anxiety, tension, irritability, and restlessness associated with nicotine withdrawal (Glassman et al, 1984).…”

Section: Discussionmentioning

confidence: 90%

The α2-adrenergic receptor agonist, clonidine, reduces alcohol drinking in alcohol-preferring (P) rats

Rasmussen

Alexander

Malone

et al. 2014

Alcohol

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Evidence suggests that noradrenergic signaling may play a role in mediating alcohol-drinking behavior in both rodents and humans. We have investigated this possibility by administering clonidine to alcohol-drinking rats selectively bred for alcohol preference (P line). Clonidine is an α2-adrenergic receptor agonist which, at low doses, inhibits noradrenergic signaling by decreasing norepinephrine release from presynaptic noradrenergic neurons. Adult male P rats were given 24-h access to food and water and scheduled access to a 15% (v/v) alcohol solution for 2 h daily. Rats received intraperitoneal (IP) injections with clonidine (0, 10, 20, 40, or 80 µg/kg body weight [BW], 10–11 rats/treatment group) once/day at 30 min prior to onset of the daily 2-h alcohol access period for 2 consecutive days. Clonidine, in doses of 40 or 80 µg/kg BW, significantly reduced alcohol intake on both days of treatment (p < 0.001). Two weeks later, rats were treated with clonidine for 5 consecutive days and clonidine, in doses of 40 or 80 µg/kg BW, reduced alcohol intake on all 5 treatment days (p < 0.001). Clonidine did not alter water consumption during the daily 2-h free-choice between alcohol and water. In a separate group of male P rats, clonidine (40 µg/kg BW) suppressed intake of a saccharin solution (0.04 g/L). These results are consistent with and complement our previous findings that the α1-adrenergic receptor antagonist, prazosin, decreases voluntary alcohol drinking in alcohol-preferring rats, but suggests that effects of clonidine may not be specific for alcohol. The results suggest that although activation of the noradrenergic system plays an important role in mediating voluntary alcohol drinking, care is needed in selecting which drugs to use to suppress central noradrenergic signaling in order to maximize the selectivity of the drugs for treating alcohol-use disorders.

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“…Clonidine is a central sympatholytic drug which decreases presynaptic alpha-2 receptors in the locus coeruleus and is an effective treatment for opioid withdrawal. 15,[17][18][19] Even if this treatment was safe and effective in our case, we recommend prudence before considering the option of clonidine therapy in patients suffering from LV dysfunction because it can reduce the cardiac output due to its anti-adrenegic effect. Further studies on larger groups of patients are needed to properly assess the safety and efficacy profile of clonidine in treatment of TTC due to opioid withdrawal.…”

Section: Discussionmentioning

confidence: 99%

Heart failure due to ‘stress cardiomyopathy’: a severe manifestation of the opioid withdrawal syndrome

Spadotto

Zorzi

ElMaghawry

et al. 2013

European Heart Journal: Acute Cardiovascular Care

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Takotsubo cardiomyopathy (TTC) is a transient left ventricular (LV) dysfunction due to akinesia of the LV mid-apical segments ('apical ballooning') in the absence of critical coronary stenoses which can be complicated in the acute phase by heart failure, mitral regurgitation, life-threatening ventricular arrhythmias, or apical LV thrombosis. The syndrome is typically precipitated by intense emotional or physical stress; however, other causes of sympathetic overstimulation including administration of exogenous sympathomimetics or withdrawal of sympathetic antagonists can trigger TTC. We report the case of a patient who unexpectedly developed an 'apical ballooning' with severe reduction in the LV systolic function and heart failure after the withdrawal of methadone. The case supports the concept that increased sympathetic activity secondary to opioids withdrawal can trigger a stress-induced severe LV dysfunction. Physicians should be aware that the abrupt discontinuation of a long-term therapy with opioids may lead to serious cardiac complications. The administration of clonidine may be considered to prevent early clinical manifestations of addictive withdrawal, including TTC.

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THE NEUROBIOLOGICAL IMPLICATIONS OF CLONIDINE HCl

Cited by 36 publications

References 46 publications

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

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

The α2-adrenergic receptor agonist, clonidine, reduces alcohol drinking in alcohol-preferring (P) rats

Heart failure due to ‘stress cardiomyopathy’: a severe manifestation of the opioid withdrawal syndrome

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