Ability of angiotensin II to modulate striatal dopamine release via the AT1 receptor in vitro and in vivo

Brown, D. C.; Steward, Lucinda J.; Jin, G.; Barnes, NM

doi:10.1111/j.1476-5381.1996.tb15418.x

Cited by 107 publications

(60 citation statements)

References 50 publications

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“…Furthermore antagonist of AT1Rs has been shown to be neuroprotective [116]. Interaction between AII and DA was suggested by early microdialysis studies, which showed that acute AII perfusion induces DA release and the effect was blocked by AT1Rs antagonists [106,117]. The mechanism responsible for the AII induced DA release has not been completely clarified, although it's been thought that involvement of D2 auto-receptors could be participating [106].…”

Section: Renin-angiotensin Systemmentioning

confidence: 99%

Dopamine Receptors and Neurodegeneration

Rangel‐Barajas¹,

Coronel²,

Florán³

2015

Aging and disease

191

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Dopamine (DA) is one of the major neurotransmitters and participates in a number of functions such as motor coordination, emotions, memory, reward mechanism, neuroendocrine regulation etc. DA exerts its effects through five DA receptors that are subdivided in 2 families: D1-like DA receptors (D1 and D5) and the D2-like (D2, D3 and D4). All DA receptors are widely expressed in the central nervous system (CNS) and play an important role in not only in physiological conditions but also pathological scenarios. Abnormalities in the DAergic system and its receptors in the basal ganglia structures are the basis Parkinson's disease (PD), however DA also participates in other neurodegenerative disorders such as Huntington disease (HD) and multiple sclerosis (MS). Under pathological conditions reorganization of DAergic system has been observed and most of the times, those changes occur as a mechanism of compensation, but in some cases contributes to worsening the alterations. Here we review the changes that occur on DA transmission and DA receptors (DARs) at both levels expression and signals transduction pathways as a result of neurotoxicity, inflammation and in neurodegenerative processes. The better understanding of the role of DA receptors in neuropathological conditions is crucial for development of novel therapeutic approaches to treat alterations related to neurodegenerative diseases.

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Section: Renin-angiotensin Systemmentioning

confidence: 99%

Dopamine Receptors and Neurodegeneration

Rangel‐Barajas¹,

Coronel²,

Florán³

2015

Aging and disease

191

View full text Add to dashboard Cite

show abstract

“…The brain possesses a local angiotensin system (Gendron et al, 2003;McKinley et al, 2003;Pan, 2004;Rodriguez-Pallares et al, 2004), and the results of previous studies have suggested that AII and its receptors play an important role in modulating striatal dopamine (DA) levels. Both AII and AII receptors as well as angiotensinogen and angiotensin-converting enzyme (ACE) have been observed in the striatum (Quinlan and Phillips, 1981;Brownfield et al, 1982;Chai et al, 1987;Allen et al, 1992Allen et al, , 1998, and AII stimulates the release of newly synthesized DA via angiotensin type 1 receptors (AT 1 ) located in the striatal DA terminals (Mendelsohn et al, 1993;Brown et al, 1996;Ge and Barnes 1996). However, it has recently been shown that in several cell types, including neurons, reactive oxygen species (ROS) play a crucial role in the signaling of AII via AT 1 receptors.…”

mentioning

confidence: 98%

Angiotensin‐converting enzyme inhibition reduces oxidative stress and protects dopaminergic neurons in a 6‐hydroxydopamine rat model of Parkinsonism

Lopez-Real

Rey

Soto‐Otero

et al. 2005

J of Neuroscience Research

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It is now established that the brain possesses a local renin-angiotensin system and that angiotensin II exerts multiple actions in the nervous system, including regulation of striatal dopamine release. Furthermore, angiotensin activates NADPH-dependent oxidases, which are a major source of superoxide, and angiotensin-converting enzyme inhibitors, commonly used in the treatment of hypertension and chronic heart failure, have shown antioxidant properties in several tissues. Oxidative stress is a key contributor to the pathogenesis and progression of Parkinson's disease. In the present study, we treated rats with intraventricular injections of the dopaminergic neurotoxin 6-hydroxydopamine and subcutaneous injections of the angiotensin-converting enzyme inhibitor Captopril to study the possible neuroprotective effect of the latter on the dopaminergic system and on 6-hydroxydopamine-induced oxidative stress. Rats treated with Captopril and 6-hydroxydopamine showed significantly less reduction in the number of dopaminergic neurons (i.e., immunoreactive to tyrosine hydroxylase) in the substantia nigra and in the density of striatal dopaminergic terminals than 6-hydroxydopamine-lesioned rats not treated with Captopril. In addition, Captopril reduced the levels of major oxidative stress indicators (i.e., lipid peroxidation and protein oxidation) in the ventral midbrain and the striatum of 6-hydroxydopamine-lesioned rats. Our results suggest that angiotensin-converting enzyme inhibitors may be useful for treatment of Parkinson's disease and that further investigation should focus on the neuroprotective capacity of these compounds.

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“…14 For example, when angiotensin II was introduced by microdialysis into the striatum, the level of dopamine increased to three times baseline. 15 On the other hand, stimulation of the angiotensin type 2 (AT 2 ) receptor, which has been expected to play a protective role in RAS.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin II type 2 receptor signaling affects dopamine levels in the brain and prevents binge eating disorder

Nakaoka

Mogi

Kanno

et al. 2015

J Renin Angiotensin Aldosterone Syst

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Introduction: Binge eating disorder (BED) is associated with dopaminergic activation as food reward, resulting in metabolism-related disorders. Stimulation of angiotensin type 2 (AT2) receptor is reported to inhibit dopamine synthesis. We investigated the possible roles of AT2 receptor-mediated dopamine regulation in the pathogenesis of BED. Materials and methods: Male C57BL/6 mice, type 2 diabetic (KKAy) mice and AT2 receptor-null (AT2KO) mice at eight weeks old were treated with AT2 receptor agonist, compound 21 (C21) or saline for two weeks. Mice were subjected to fasting for two days followed by re-feeding for seven days. Results: Treatment with C21 attenuated the rebound proportion of body weight, food intake and water intake in KKAy mice, but not in C57BL/6 and AT2KO mice. Dopamine concentration in the striatum was further increased by fasting in KKAy and AT2KO mice. Administration of C21 significantly attenuated this fasting-induced increase in dopamine level only in KKAy mice. Dopamine receptor D1, D2 expression in the substantia nigra were markedly lower in KKAy mice compared with C57BL/6 mice, while administration of C21 increased their expression in KKAy mice. Conclusions: Our study suggests that AT2 receptor stimulation may be a new therapeutic approach to improve eating disorder associated with dopamine resistance.

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Ability of angiotensin II to modulate striatal dopamine release via the AT₁ receptor in vitro and in vivo

Cited by 107 publications

References 50 publications

Dopamine Receptors and Neurodegeneration

Dopamine Receptors and Neurodegeneration

Angiotensin‐converting enzyme inhibition reduces oxidative stress and protects dopaminergic neurons in a 6‐hydroxydopamine rat model of Parkinsonism

Angiotensin II type 2 receptor signaling affects dopamine levels in the brain and prevents binge eating disorder

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