The Renin-Angiotensin System and the Cerebrovascular Diseases: Experimental and Clinical Evidence

2020 ◽  
Vol 27 (6) ◽  
pp. 463-475 ◽  
Author(s):  
Lucas M. Kangussu ◽  
Lucas Alexandre Santos Marzano ◽  
Cássio Ferraz Souza ◽  
Carolina Couy Dantas ◽  
Aline Silva Miranda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Renin Angiotensin System ◽  
Cerebrovascular Diseases ◽  
Therapeutic Effects ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Mas Receptor

Cerebrovascular Diseases (CVD) comprise a wide spectrum of disorders, all sharing an acquired or inherited alteration of the cerebral vasculature. CVD have been associated with important changes in systemic and tissue Renin-Angiotensin System (RAS). The aim of this review was to summarize and to discuss recent findings related to the modulation of RAS components in CVD. The role of RAS axes is more extensively studied in experimentally induced stroke. By means of AT1 receptors in the brain, Ang II hampers cerebral blood flow and causes tissue ischemia, inflammation, oxidative stress, cell damage and apoptosis. On the other hand, Ang-(1-7) by stimulating Mas receptor promotes angiogenesis in brain tissue, decreases oxidative stress, neuroinflammation, and improves cognition, cerebral blood flow, neuronal survival, learning and memory. In regard to clinical studies, treatment with Angiotensin Converting Enzyme (ACE) inhibitors and AT1 receptor antagonists exerts preventive and therapeutic effects on stroke. Besides stroke, studies support a similar role of RAS molecules also in traumatic brain injury and cerebral aneurysm. The literature supports a beneficial role for the alternative RAS axis in CVD. Further studies are necessary to investigate the therapeutic potential of ACE2 activators and/or Mas receptor agonists in patients with CVD.

Splanchnic blood flow and hepatic glucose production in exercising humans: role of renin-angiotensin system

2001 ◽  
Vol 281 (6) ◽  
pp. R1854-R1861 ◽  
Author(s):  
Raynald Bergeron ◽  
Michael Kjær ◽  
Lene Simonsen ◽  
Jens Bülow ◽  
Dorthe Skovgaard ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renin Angiotensin System ◽  
Glucose Production ◽  
Splanchnic Blood Flow ◽  
Control Group ◽  
Moderate Exercise ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin

The study examined the implication of the renin-angiotensin system (RAS) in regulation of splanchnic blood flow and glucose production in exercising humans. Subjects cycled for 40 min at 50% maximal O2 consumption (V˙o 2 max) followed by 30 min at 70% V˙o 2 maxeither with [angiotensin-converting enzyme (ACE) blockade] or without (control) administration of the ACE inhibitor enalapril (10 mg iv). Splanchnic blood flow was estimated by indocyanine green, and splanchnic substrate exchange was determined by the arteriohepatic venous difference. Exercise led to an ∼20-fold increase ( P < 0.001) in ANG II levels in the control group (5.4 ± 1.0 to 102.0 ± 25.1 pg/ml), whereas this response was blunted during ACE blockade (8.1 ± 1.2 to 13.2 ± 2.4 pg/ml) and in response to an orthostatic challenge performed postexercise. Apart from lactate and cortisol, which were higher in the ACE-blockade group vs. the control group, hormones, metabolites, V˙o 2, and RER followed the same pattern of changes in ACE-blockade and control groups during exercise. Splanchnic blood flow (at rest: 1.67 ± 0.12, ACE blockade; 1.59 ± 0.18 l/min, control) decreased during moderate exercise (0.78 ± 0.07, ACE blockade; 0.74 ± 0.14 l/min, control), whereas splanchnic glucose production (at rest: 0.50 ± 0.06, ACE blockade; 0.68 ± 0.10 mmol/min, control) increased during moderate exercise (1.97 ± 0.29, ACE blockade; 1.91 ± 0.41 mmol/min, control). Refuting a major role of the RAS for these responses, no differences in the pattern of change of splanchnic blood flow and splanchnic glucose production were observed during ACE blockade compared with controls. This study demonstrates that the normal increase in ANG II levels observed during prolonged exercise in humans does not play a major role in the regulation of splanchnic blood flow and glucose production.

scholarly journals Vitamin D Deficiency Aggravates Nephrotoxicity, Hypertension and Dyslipidemia Caused by Tenofovir: Role of Oxidative Stress and Renin-Angiotensin System

PLoS ONE ◽  
2014 ◽  
Vol 9 (7) ◽  
pp. e103055 ◽  
Author(s):  
Daniele Canale ◽  
Ana Carolina de Bragança ◽  
Janaína Garcia Gonçalves ◽  
Maria Heloisa Massola Shimizu ◽  
Talita Rojas Sanches ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Vitamin D Deficiency ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Role of renin-angiotensin system antagonists in the control of hepatic blood flow and liver protection

1998 ◽  
Vol 114 ◽  
pp. A1230
Author(s):  
K. Czarnobilski ◽  
T. Pawlik ◽  
R. Sendur ◽  
M. Zejc-Bajsarowicz ◽  
W.W. Pawlik
Keyword(s):  
Blood Flow ◽  
Hepatic Blood Flow ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Liver Protection

Effect of angiotensin II antagonist infusion on autoregulation of renal blood flow

1976 ◽  
Vol 231 (4) ◽  
pp. 1267-1271 ◽  
Author(s):  
Y Abe ◽  
T Kishimoto ◽  
K Yamamoto
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Renin Angiotensin System ◽  
Pressure Reduction ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renal Autoregulation ◽  
Angiotensin Ii Antagonist

The role of the renin-angiotensin system in the autoregulation of renal blood flow was examined in the anesthetized dog. The angiotensin II antagonist, [1-sarcosine, 8-isoleucine]angiotensin II, was continuously infused into the renal artery at rates of 1 and 3 mug/min, and renin secretion rate and intrarenal distribution of blood flow as well as total renal blood flow were measured during acute reductions in renal perfusion pressure within and below the range of autoregulation. Renal autoregulation and redistribution of blood flow by pressure reduction were not disturbed by the angiotensin II antagonist. This result does not provide any evidence for a primary role of the renin-angiotensin system in renal autoregulation. Redistribution of blood flow by pressure reduction occurred independently of the renin-angiotensin system. It might depend on the differences in the resting tone among the zones.

scholarly journals Renin Angiotensin System Gene Polymorphisms and Cerebral Blood Flow Regulation

Stroke ◽  
2010 ◽  
Vol 41 (4) ◽  
pp. 635-640 ◽  
Author(s):  
Ihab Hajjar ◽  
Farzaneh Sorond ◽  
Yi-Hsiang Hsu ◽  
Andrew Galica ◽  
L. Adrienne Cupples ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Gene Polymorphisms ◽  
Renin Angiotensin System ◽  
Flow Regulation ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Blood Flow Regulation

The effects of increased dietary salt on renal blood flow responses during physiological stress: Role of renin‐angiotensin system

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Afsana Momen ◽  
Cheryl Blaha ◽  
Karen Thomas ◽  
Amir Gahremanpour ◽  
Kristen S. Gray ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Physiological Stress ◽  
Renin Angiotensin System ◽  
Dietary Salt ◽  
Angiotensin System ◽  
Renin Angiotensin

Bradykinin-induced renal hemodynamic alterations: renin and prostaglandin relationships

1979 ◽  
Vol 237 (6) ◽  
pp. F433-F440 ◽  
Author(s):  
W. Flamenbaum ◽  
J. Gagnon ◽  
P. Ramwell
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Competitive Inhibition ◽  
Renin Angiotensin System ◽  
Prostaglandin Synthetase ◽  
Secretory Rate ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Prostaglandin Release

The present studies examined the role of the renin-angiotensin system as a modifier of the renal vasomotor response to bradykinin. Renal arterial bradykinin infusion (80 ng.kg-1.min-1) initially resulted in increased renal blood flow (RBF). The secretory rates of renin and prostaglandins increased after 60 min. With continued bradykinin administration (120 min) RBF and prostaglandin secretory rates returned toward control values, although renin secretory rate remained elevated (P less than 0.02). After prostaglandin synthetase inhibition, RBF decreased and bradykinin administration returned RBF to control values. Prostaglandin secretory rates decreased after meclofenamate (P less than 0.005). Continued bradykinin infusion resulted in a return of the renin secretory rate to control values. The administration of bradykinin after competitive inhibition of angiotensin II resulted in a sustained increase in renal blood flow. These results suggest that the initial bradykinin-induced renal hyperemia is only partially dependent on enhanced prostaglandin release, the increase in renin secretion by bradykinin infusion after prostaglandin synthetase inhibition is consistent with a bradykinin and renin interaction, and the lack of a sustained hyperemia after bradykinin is related to increased renin-angiotensin system activity.

scholarly journals The role of the renin-angiotensin system in atrial fibrillation and the therapeutic effects of ACE-Is and ARBS

2008 ◽  
Vol 66 (3) ◽  
pp. 345-351 ◽  
Author(s):  
Giuseppina Novo ◽  
Daniela Guttilla ◽  
Giovanni Fazio ◽  
Debbie Cooper ◽  
Salvatore Novo
Keyword(s):  
Atrial Fibrillation ◽  
Renin Angiotensin System ◽  
Therapeutic Effects ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Mitochondria-Endoplasmic Reticulum Crosstalk in Parkinson’s Disease: The Role of Brain Renin Angiotensin System Components

Biomolecules ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1669
Author(s):  
Tuladhar Sunanda ◽  
Bipul Ray ◽  
Arehally M. Mahalakshmi ◽  
Abid Bhat ◽  
Luay Rashan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Endoplasmic Reticulum ◽  
Neurodegenerative Diseases ◽  
Calcium Homeostasis ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

The past few decades have seen an increased emphasis on the involvement of the mitochondrial-associated membrane (MAM) in various neurodegenerative diseases, particularly in Parkinson’s disease (PD) and Alzheimer’s disease (AD). In PD, alterations in mitochondria, endoplasmic reticulum (ER), and MAM functions affect the secretion and metabolism of proteins, causing an imbalance in calcium homeostasis and oxidative stress. These changes lead to alterations in the translocation of the MAM components, such as IP3R, VDAC, and MFN1 and 2, and consequently disrupt calcium homeostasis and cause misfolded proteins with impaired autophagy, distorted mitochondrial dynamics, and cell death. Various reports indicate the detrimental involvement of the brain renin–angiotensin system (RAS) in oxidative stress, neuroinflammation, and apoptosis in various neurodegenerative diseases. In this review, we attempted to update the reports (using various search engines, such as PubMed, SCOPUS, Elsevier, and Springer Nature) demonstrating the pathogenic interactions between the various proteins present in mitochondria, ER, and MAM with respect to Parkinson’s disease. We also made an attempt to speculate the possible involvement of RAS and its components, i.e., AT1 and AT2 receptors, angiotensinogen, in this crosstalk and PD pathology. The review also collates and provides updated information on the role of MAM in calcium signaling, oxidative stress, neuroinflammation, and apoptosis in PD.

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