Angiotensin II reduces voluntary alcohol intake in the rat

Grupp, Larry A.; Killian, M; Perlanski, E.; Stewart, Robert B.

doi:10.1016/0091-3057(88)90007-x

Cited by 49 publications

(9 citation statements)

References 12 publications

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“…The observation that TGM123 mice exhibited increased alcohol consumption is in accordance with findings of Fitts (4), who described increased alcohol intake upon intracerebroventricular infusion of AII in rats. Other authors reported a reduction of alcohol intake induced by exogenously administered AII in rats (7,8). These experiments, however, employed a different mode of administration of the alcoholic beverage.…”

Section: Discussionmentioning

confidence: 97%

Alcohol consumption is controlled by angiotensin II

Maul¹,

Siems²,

Hoehe

et al. 2001

FASEB j.

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Pharmacological manipulation of the renin‐angiotensin system (RAS) appears to alter voluntary alcohol consumption in animals. We have now addressed the role of angiotensin II (AII) in alcohol intake by comparing the alcohol‐drinking behavior of mice lacking or overexpressing the angiotensinogen gene in a two‐bottle choice paradigm. We found that alcohol consumption was directly related to AII levels. Animals harboring a rat angiotensinogen transgene consumed significantly more of the alcoholic beverage than did controls. This effect could be remarkably reduced by spirapril, an inhibitor of the angiotensin‐converting enzyme (ACE). However, mice lacking the angiotensinogen gene exhibited a markedly reduced alcohol intake. These results indicate a role for the angiotensinogen gene in alcohol consumption via modulation of AII.

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Section: Discussionmentioning

confidence: 97%

Alcohol consumption is controlled by angiotensin II

Maul¹,

Siems²,

Hoehe

et al. 2001

FASEB j.

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“…1987) and was hypothesized to be involved in alcohol consumption and preference. A series of studies showed that angiotensin II injected systemically and intracerebroventricularly increased ethanol intake in rats (Grupp et al . 1988; Fitts 1993) and mice (Weisinger et al .…”

Section: Neuropeptide Y and Other Neuropeptides (Table 12)mentioning

confidence: 99%

REVIEW: Alcohol‐related genes: contributions from studies with genetically engineered mice

Crabbe

Phillips

Harris³

et al. 2006

Addiction Biology

216

175

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Since 1996, nearly 100 genes have been studied for their effects related to ethanol in mice using genetic modifications including gene deletion, gene overexpression, gene knock-in, and occasionally by studying existing mutants. Nearly all such studies have concentrated on genes expressed in brain, and the targeted genes range widely in their function, including most of the principal neurotransmitter systems, several neurohormones, and a number of signaling molecules. We review 141 published reports of effects (or lack thereof) of 93 genes on responses to ethanol. While most studies have focused on ethanol self-administration and reward, and/or sedative effects, other responses studied include locomotor stimulation, anxiolytic effects, and neuroadaptation (tolerance, sensitization, withdrawal). About 1/4 of the engineered mutations increase self-administration, 1/3 decrease it, and about 40% have no significant effect. In many cases, the effects on self-administration are rather modest and/or depend on the specific experimental procedures. In some cases, genes in the background strains on which the mutant is placed are important for results. Not surprisingly, review of the systems affected further supports roles for serotonin, gamma-aminobutyric acid, opioids and dopamine, all of which have long been foci of alcohol research. Novel modulatory effects of protein kinase C and G protein-activated inwardly rectifying K+ (GIRK) channels are also suggested. Some newer research with cannabinoid systems is promising, and has led to ongoing clinical trials.

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“…In addition, MCH is reported to increase fluid intake (Clegg et al, 2003) and decrease anxiety (Kela et al, 2003;Monzon and De Barioglio, 1999;Monzon et al, 2001). Importantly, the regulation of energy homeostasis, fluid balance, and anxiety have all been implicated in the etiology of alcoholism (Grupp et al, 1988;Grupp et al, 1989;Markou et al, 1998;Swendsen and Merikangas, 2000;Swendsen et al, 1998;Thiele et al, 2003;Thomas et al, 2003). Moreover, the anatomical distribution of MCH-producing neurons and MCH receptors is indicative of involvement in reward and motivation.…”

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confidence: 99%