Both Nox2‐ and Nox4‐containing NAD(P)H oxidases are required for the full vasopressor effects of angiotensin‐II (Ang‐II) in the central nervous system

Background: The Renin-Angiotensin System (RAS) is a key regulator of cardiovascular and renal homeostasis, but also plays important roles in mediating physiological functions in the central nervous system (CNS). The effects of the RAS were classically described as mediated by angiotensin (Ang) II via angiotensin type 1 (AT1) receptors. However, another arm of the RAS formed by the angiotensin converting enzyme 2 (ACE2), Ang-(1-7) and the Mas receptor has been a matter of investigation due to its important physiological roles, usually counterbalancing the classical effects exerted by Ang II. Objective: We aim to provide an overview of effects elicited by the RAS, especially Ang-(1-7), in the brain. We also aim to discuss the therapeutic potential for neuropsychiatric disorders for the modulation of RAS. Method: We carried out an extensive literature search in PubMed central. Results: Within the brain, Ang-(1-7) contributes to the regulation of blood pressure by acting at regions that control cardiovascular functions. In contrast with Ang II, Ang-(1-7) improves baroreflex sensitivity and plays an inhibitory role in hypothalamic noradrenergic neurotransmission. Ang-(1-7) not only exerts effects related to blood pressure regulation, but also acts as a neuroprotective component of the RAS, for instance, by reducing cerebral infarct size, inflammation, oxidative stress and neuronal apoptosis. Conclusion: Pre-clinical evidence supports a relevant role for ACE2/Ang-(1-7)/Mas receptor axis in several neuropsychiatric conditions, including stress-related and mood disorders, cerebrovascular ischemic and hemorrhagic lesions and neurodegenerative diseases. However, very few data are available regarding the ACE2/Ang-(1-7)/Mas receptor axis in human CNS.

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Central site for pressor action of blood-borne angiotensin in rat

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1980.239.3.r358 ◽

1980 ◽

Vol 239 (3) ◽

pp. R358-R361 ◽

Cited By ~ 5

Author(s):

G. D. Fink ◽

J. R. Haywood ◽

W. J. Bryan ◽

W. Packwood ◽

M. J. Brody

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Angiotensin Ii ◽

Pressor Response ◽

Third Ventricle ◽

Central Component ◽

The Third ◽

Electrolytic Lesions ◽

The Central Nervous System ◽

The Difference

A previous study demonstrated that the threshold dose of intra-arterial angiotensin II required to induce a pressor response in the rat was significantly lower when the drug was administered into the carotid artery than when administered into the abdominal aorta. This result was interpreted to indicate that part of the increase in arterial pressure produced by low concentrations of blood-borne angiotensin in this species was the result of an effect on structures in the central nervous system selectively accessible via the carotid vascular bed. The purpose of the present study was to establish more precisely the site of the pressor action of angiotensin within the central nervous system. The central component of the pressor effect of angiotensin was quantified as the difference in pressor responses to intracarotid and intra-aortic infusions of angiotensin II (delta c-a). In conscious rats, delta c-a was attenuated by administration of the angiotensin antagonist, saralasin, into the third cerebral ventricle. In rats with chronic electrolytic lesions of the anteroventral third ventricle (AV3V), delta c-a was abolished. Periventricular structures surrounding the third ventricle appear to mediate the central component of the pressor action of blood-borne angiotensin in the rat.

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Neuroanatomical distribution of angiotensin-II-like neuropeptide within the central nervous system of the crab Chasmagnathus; physiological changes triggered by water deprivation

Cell and Tissue Research ◽

10.1007/s00441-010-0990-8 ◽

2010 ◽

Vol 341 (1) ◽

pp. 181-195 ◽

Cited By ~ 9

Author(s):

Lia Frenkel ◽

Beatriz Dimant ◽

Enrique L. Portiansky ◽

Hans Imboden ◽

Héctor Maldonado ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Angiotensin Ii ◽

Water Deprivation ◽

Physiological Changes ◽

The Central Nervous System

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Angiotensin II and angiotensin-1-7 redox signaling in the central nervous system

Current Opinion in Pharmacology ◽

10.1016/j.coph.2011.01.001 ◽

2011 ◽

Vol 11 (2) ◽

pp. 138-143 ◽

Cited By ~ 31

Author(s):

Matthew C Zimmerman

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Angiotensin Ii ◽

Redox Signaling ◽

The Central Nervous System

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Superoxide Mediates the Actions of Angiotensin II in the Central Nervous System

Circulation Research ◽

10.1161/01.res.0000043501.47934.fa ◽

2002 ◽

Vol 91 (11) ◽

pp. 1038-1045 ◽

Cited By ~ 308

Author(s):

Matthew C. Zimmerman ◽

Eric Lazartigues ◽

Julie A. Lang ◽

Puspha Sinnayah ◽

Iman M. Ahmad ◽

...

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Angiotensin Ii ◽

The Central Nervous System

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Central Nervous System Pressor Responses in Rats Susceptible and Resistant to Sodium Chloride Hypertension

Clinical Science ◽

10.1042/cs055225s ◽

1978 ◽

Vol 55 (s4) ◽

pp. 225s-227s ◽

Cited By ~ 11

Author(s):

T. Ikeda ◽

L. Tobian ◽

J. Iwai ◽

Patricia Goossens

Keyword(s):

Blood Pressure ◽

Central Nervous System ◽

Nervous System ◽

Sodium Chloride ◽

Angiotensin Ii ◽

Hypertonic Saline ◽

Pressor Effect ◽

Left Lateral Ventricle ◽

Pressor Responses ◽

The Central Nervous System

1. The pressor responses to hypertonic saline and angiotensin II introduced into the left lateral ventricle were both significantly greater in salt-sensitive (S) rats compared with salt-resistant (R) rats, with all rats on a low Na diet. 2. When S rats were given thiazide to nullify the pressor effect of dietary NaCl, their blood pressure averaged only 5 mmHg higher than that of the R rats; nevertheless, these S rats had significantly higher central nervous system pressor responses to angiotensin II and hypertonic saline. 3. Thus, if excessive dietary Na increases blood pressure by way of action on the central nervous system, these heightened pressor responses could partially account for the NaCl hypertension in S rats. Alternatively, depressed central nervous system pressor responses in R rats could partially explain the resistance of R rats to NaCl hypertension.

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