Actions of angiotensin II on the brain: mechanisms and physiologic role

1984 ◽  
Vol 246 (5) ◽  
pp. F533-F543 ◽  
Author(s):  
I. A. Reid
Keyword(s):  
Angiotensin Ii ◽  
Large Body ◽  
Renin Angiotensin System ◽  
Circumventricular Organs ◽  
Acth Stimulation ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Receptor Sites ◽  
The Brain

Angiotensin II acts on the brain to produce a variety of effects including elevation of arterial blood pressure, increased release of vasopressin and ACTH, stimulation of drinking and sodium appetite, and natriuresis. Many, and possibly all, of these effects can be produced by centrally administered angiotensin II or by circulating angiotensin II, which appear to act at common receptor sites located in the circumventricular organs. Whether these effects are normally produced by blood-borne angiotensin II formed by the renal renin-angiotensin system, by angiotensin II formed centrally by the putative brain renin-angiotensin system, or by both, remains to be determined. A large body of information concerning the site and mechanism of these different central actions of angiotensin II is available, and the physiologic significance of these actions is beginning to be understood. Nevertheless, much additional research will be required before the actions of angiotensin II on the brain are completely understood.

Coevolution of the rennin–angiotensin system and the nervous control of blood circulation

1984 ◽  
Vol 62 (2) ◽  
pp. 137-147 ◽  
Author(s):  
John X. Wilson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Renin Angiotensin System ◽  
Peripheral Vascular Resistance ◽  
Peripheral Vascular ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood

The mammalian renin–angiotensin system appears to be involved in the maintenance of blood volume and pressure because (i) sodium depletion, hypovolemia, and hypotension increase renin levels, and (ii) administration of exogenous angiotensin II rapidly increases mineralocorticoid and antidiuretic hormone production, transepithelial ion transport, drinking behavior, and peripheral vascular resistance. Are these also the physiological properties of the renin–angiotensin system in nonmammalian species? Signals for altered levels of renin activity have yet to be conclusively identified in nonmammalian vertebrates, but circulating renin levels are elevated by hypotension in teleost fish and birds. Systemic injection of angiotensin II causes an increase in arterial blood pressure in all the vertebrates studied, suggesting that barostatic control is a universal function of this hormone. Angiotensin II alters vascular tone by direct action on arteriolar muscles in some species, but at concentrations of the hormone which probably are unphysiological. More generally, angiotensin II increases blood pressure indirectly, by acting on the sympathetic nervous system. Catecholamines, derived from chromaffin cells and (or) from peripheral adrenergic nerves, mediate some portion of the vasopressor response to angiotensin II in cyclostomes, elasmobranchs, teleosts, amphibians, reptiles, mammals, and birds. Alteration of sympathetic outflow is a prevalent mechanism through which the renin–angiotensin system may integrate blood volume, cardiac output, and peripheral vascular resistance to achieve control of blood pressure and adequate perfusion of tissues.

scholarly journals The Renin–Angiotensin System Modulates Dopaminergic Neurotransmission: A New Player on the Scene

2021 ◽  
Vol 13 ◽  
Author(s):  
Tamara Kobiec ◽  
Matilde Otero-Losada ◽  
Guenson Chevalier ◽  
Lucas Udovin ◽  
Sofía Bordet ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Dopaminergic Neurons ◽  
Neuronal Degeneration ◽  
Renin Angiotensin System ◽  
Receptor Activation ◽  
World Population ◽  
Major Health Problem ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain

Parkinson’s disease (PD) is an extrapyramidal disorder characterized by neuronal degeneration in several regions of the peripheral and central nervous systems. It is the second most frequent neurodegenerative disease after Alzheimer’s. It has become a major health problem, affecting 1% of the world population over 60 years old and 3% of people beyond 80 years. The main histological findings are intracellular Lewy bodies composed of misfolded α-synuclein protein aggregates and loss of dopaminergic neurons in the central nervous system. Neuroinflammation, apoptosis, mitochondrial dysfunction, altered calcium homeostasis, abnormal protein degradation, and synaptic pathobiology have been put forward as mechanisms leading to cell death, α-synuclein deposition, or both. A progressive loss of dopaminergic neurons in the substantia nigra late in the neurodegeneration leads to developing motor symptoms like bradykinesia, tremor, and rigidity. The renin–angiotensin system (RAS), which is involved in regulating blood pressure and body fluid balance, also plays other important functions in the brain. The RAS is involved in the autocrine and paracrine regulation of the nigrostriatal dopaminergic synapses. Dopamine depletion, as in PD, increases angiotensin II expression, which stimulates or inhibits dopamine synthesis and is released via AT1 or AT2 receptors. Furthermore, angiotensin II AT1 receptors inhibit D1 receptor activation allosterically. Therefore, the RAS may have an important modulating role in the flow of information from the brain cortex to the basal ganglia. High angiotensin II levels might even aggravate neurodegeneration, activating the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex, which leads to increased reactive oxygen species production.

Effect of methylprednisolone upon arterial pressure and the renin angiotensin system in the rat

1975 ◽  
Vol 228 (2) ◽  
pp. 613-617 ◽  
Author(s):  
LR Krakoff ◽  
R Selvadurai ◽  
E Sutter
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Substrate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Significant Fall ◽  
Arterial Blood ◽  
Methylprednisolone Treatment

The effect of methylprednisolone or deoxycorticosterone upon systemic arterial blood pressure and components of the renin-angiotensin system was studied in the rat. Rats maintained on regular diets given methylprednisolone suspension 20 mg/kg body wt demonstrated a significant increase in arterial pressure of + 37 plus or minus 5 mmHg, mean plus or minus SE, over a 2-wk period, whereas those treated with DOC and untreated controls showed no significant change. On normal diets, plasma renin concentration (PRC) of methylprednisolone-treated rats was significantly higher than that of DOC-treated rats. Methylprednisolone treatment also resulted in a significant elevation of plasma renin substrate concentration (PRS). Calculated plasma renin activity (PRA) was highest in methylprednisolone-treated rats, significantly above that of the DOC and no-steroid groups. NaCl supplementation resulted in a significant fall in PRC and PRA in all three groups; however, PRS remained significantly above normal in the methylprednisolone-treated rats. The pressor effect of angiotensin II was slightly increased in methylprednisolone-treated rats. Infusion of [Sar1,Ala8]angiotensin II (P-113) in methylprednisolone-treated rats resulted in a significant fall in diastolic arterial pressure. The results imply that methylprednisolone hypertension in the rat may be in part angiotensin dependent.

scholarly journals The Renin-Angiotensin System Modulates Inflammatory Processes in Atherosclerosis: Evidence from Basic Research and Clinical Studies

2009 ◽  
Vol 2009 ◽  
pp. 1-13 ◽  
Author(s):  
Fabrizio Montecucco ◽  
Aldo Pende ◽  
François Mach
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Basic Research ◽  
Angiotensin Ii Receptor ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renin Inhibitors ◽  
Arterial Blood ◽  
Inflammatory Processes

Recent evidence shows that the renin-angiotensin system is a crucial player in atherosclerotic processes. The regulation of arterial blood pressure was considered from its first description of the main mechanism involved. Vasoconstriction (mediated by angiotensin II) and salt and water retention (mainly due to aldosterone) were classically considered as pivotal proatherosclerotic activities. However, basic research and animal studies strongly support angiotensin II as a proinflammatory mediator, which directly induces atherosclerotic plaque development and heart remodeling. Furthermore, angiotensin II induces proatherosclerotic cytokine and chemokine secretion and increases endothelial dysfunction. Accordingly, the pharmacological inhibition of the renin-angiotensin system improves prognosis of patients with cardiovascular disease even in settings of normal baseline blood pressure. In the present review, we focused on angiotensin-convertingenzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), and renin inhibitors to update the direct activities of the renin-angiotensin system in inflammatory processes governing atherosclerosis.

scholarly journals The Brain Renin-Angiotensin System Modulates Angiotensin II–Induced Hypertension and Cardiac Hypertrophy

Hypertension ◽  
2000 ◽  
Vol 35 (1) ◽  
pp. 409-412 ◽  
Author(s):  
Ovidiu Baltatu ◽  
José Antonio Silva ◽  
Detlev Ganten ◽  
Michael Bader
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Induced Hypertension ◽  
The Brain

Central interaction of the brain atrial natriuretic polypeptide (ANP) system and the brain rennin–angiotensin system in ANP secretion from heart—evidence for possible brain–heart axis

1988 ◽  
Vol 66 (3) ◽  
pp. 255-261 ◽  
Author(s):  
Hiroshi Itoh ◽  
Kazuwa Nakao ◽  
Takayuki Yamada ◽  
Narito Morii ◽  
Shozo Shiono ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Intracerebroventricular Administration ◽  
Volume Loading ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Atrial Natriuretic Polypeptide ◽  
Basal Plasma ◽  
The Brain ◽  
Atrial Natriuretic

To elucidate the involvement of the brain renin–angiotensin system and the brain atrial natriuretic polypeptide (ANP) system in the regulation of ANP secretion from the heart, the effects of intracerebroventricular administration of angiotensin II and ANP on the plasma ANP level were examined in conscious unrestrained rats. The intracerebroventricular administration of angiotensin II at doses of 100 ng and 1 μg significantly enhanced ANP secretion induced by volume-loading with 3-mL saline infusion (peak values of the plasma ANP level: control, 220 ± 57 pg/mL; 100 ng angiotensin II, 1110 ± 320 pg/mL, p < 0.01; 1 μg angiotensin II, 1055 ± 60 pg/mL, p < 0.01). The intracerebroventricular injection of angiotensin II at the same doses alone had no significant effect on the basal plasma ANP level. The enhancing effect of central angiotensin II on ANP secretion induced by volume-loading was significantly attenuated by pretreatment with the intravenous administration of the V1-receptor antagonist of vasopressin or with the intracerebroventricular administration of phentolamine. The intracerebroventricular administration of α-rANP(4–28) (5 μg) had no significant influence on the basal plasma ANP level; however, it significantly attenuated central angiotensin II potentiating effect of volume-loading induced ANP secretion. These results indicate that the brain rennin–angiotensin system regulates ANP secretion via the stimulation of vasopressin secretion and (or) via the activation of the central α-adrenergic neural pathway, and that the brain ANP system interacts with the brain renin–angiotensin system in the central modulation of ANP secretion from the heart. The result further supports the proposed antagonistic relationship between the brain ANP system and the brain renin–angiotensin system in body fluid and blood pressure homeostasis.

scholarly journals Activation of the Central Renin-Angiotensin System Causes Local Cerebrovascular Dysfunction

Stroke ◽  
2021 ◽  
Author(s):  
T. Michael De Silva ◽  
Mary L. Modrick ◽  
Justin L. Grobe ◽  
Frank M. Faraci
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Cerebral Arteries ◽  
Renin Angiotensin System ◽  
Mesenteric Arteries ◽  
Common Mechanism ◽  
Brain Health ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain

Background and Purpose: Hypertension is a leading risk factor for cerebrovascular disease and loss of brain health. While the brain renin-angiotensin system (RAS) contributes to hypertension, its potential impact on the local vasculature is unclear. We tested the hypothesis that activation of the brain RAS would alter the local vasculature using a modified deoxycorticosterone acetate (DOCA) model. Methods: C57BL/6 mice treated with DOCA (50 mg SQ; or shams) were given tap H 2 O and H 2 O with 0.9% NaCl for 1 to 3 weeks. Results: In isolated cerebral arteries and parenchymal arterioles from DOCA-treated male mice, endothelium- and nitric oxide-dependent dilation was progressively impaired, while mesenteric arteries were unaffected. In contrast, cerebral endothelial function was not significantly affected in female mice treated with DOCA. In males, mRNA expression of renal Ren1 was markedly reduced while RAS components (eg, Agt and Ace ) were increased in both brain and cerebral arteries with central RAS activation. In NZ44 reporter mice expressing GFP (green fluorescent protein) driven by the angiotensin II type 1A receptor ( Agtr1a ) promoter, DOCA increased GFP expression ≈3-fold in cerebral arteries. Impaired endothelial responses were restored to normal by losartan, an AT1R (angiotensin II type 1 receptor) antagonist. Last, DOCA treatment produced inward remodeling of parenchymal arterioles. Conclusions: These findings suggest activation of the central and cerebrovascular RAS impairs endothelial (nitric oxide dependent) signaling in brain through expression and activation of AT1R and sex-dependent effects. The central RAS may be a key contributor to vascular dysfunction in brain in a preclinical (low renin) model of hypertension. Because the brain RAS is also activated during aging and other diseases, a common mechanism may promote loss of endothelial and brain health despite diverse cause.

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