scholarly journals The Angiotensin-Melatonin Axis

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Luciana A. Campos ◽  
Jose Cipolla-Neto ◽  
Fernanda G. Amaral ◽  
Lisete C. Michelini ◽  
Michael Bader ◽  
...  
Keyword(s):  
Circadian Rhythms ◽  
Metabolic Disorders ◽  
Clock Genes ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Beneficial Effects ◽  
Progression Of Disease ◽  
The Central Nervous System ◽  
Peripheral Clocks

Accumulating evidence indicates that various biological and neuroendocrine circadian rhythms may be disrupted in cardiovascular and metabolic disorders. These circadian alterations may contribute to the progression of disease. Our studies direct to an important role of angiotensin II and melatonin in the modulation of circadian rhythms. The brain renin-angiotensin system (RAS) may modulate melatonin synthesis, a hormone with well-established roles in regulating circadian rhythms. Angiotensin production in the central nervous system may not only influence hypertension but also appears to affect the circadian rhythm of blood pressure. Drugs acting on RAS have been proven effective in the treatment of cardiovascular and metabolic disorders including hypertension and diabetes mellitus (DM). On the other hand, since melatonin is capable of ameliorating metabolic abnormalities in DM and insulin resistance, the beneficial effects of RAS blockade could be improved through combined RAS blocker and melatonin therapy. Contemporary research is evidencing the existence of specific clock genes forming central and peripheral clocks governing circadian rhythms. Further research on the interaction between these two neurohormones and the clock genes governing circadian clocks may progress our understanding on the pathophysiology of disease with possible impact on chronotherapeutic strategies.

Neuromodulatory role of angiotensin-(1–7) in the central nervous system

2013 ◽  
Vol 125 (2) ◽  
pp. 57-65 ◽  
Author(s):  
Mariela M. Gironacci ◽  
Nadia A. Longo Carbajosa ◽  
Jorge Goldstein ◽  
Bruno D. Cerrato
Keyword(s):  
Renin Angiotensin System ◽  
Cardiovascular Effects ◽  
Synaptic Cleft ◽  
Neutral Endopeptidase ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
The Central Nervous System ◽  
Release Characteristic ◽  
Transporter Expression

Ang-(1–7) [angiotensin-(1–7)] constitutes an important functional end-product of the RAS (renin–angiotensin system) endogenously formed from AngI (angiotensin I) or AngII (angiotensin II) through the catalytic activity of ACE2 (angiotensin-converting enzyme 2), prolyl carboxypeptidase, neutral endopeptidase or other endopeptidases. Ang-(1–7) lacks the pressor, dipsogenic or stimulatory effect on aldosterone release characteristic of AngII. In contrast, it produces vasodilation, natriuresis and diuresis, and inhibits angiogenesis and cell growth. At the central level, Ang-(1–7) acts at sites involved in the control of cardiovascular function, thus contributing to blood pressure regulation. This action may result from its inhibitory neuromodulatory action on NE [noradrenaline (norepinephrine)] levels at the synaptic cleft, i.e. Ang-(1–7) reduces NE release and synthesis, whereas it causes an increase in NE transporter expression, contributing in this way to central NE neuromodulation. Thus, by selective neurotransmitter release, Ang-(1–7) may contribute to the overall central cardiovascular effects. In the present review, we summarize the central effects of Ang-(1–7) and the mechanism by which the peptide modulates NE levels in the synaptic cleft. We also provide new evidences of its cerebroprotective role.

scholarly journals Stroke in SARS-CoV-2 Infection: A Pictorial Overview of the Pathoetiology

2021 ◽  
Vol 8 ◽  
Author(s):  
Saeideh Aghayari Sheikh Neshin ◽  
Shima Shahjouei ◽  
Eric Koza ◽  
Isabel Friedenberg ◽  
Faezeh Khodadadi ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Renin Angiotensin System ◽  
Cardiovascular Complications ◽  
Elevated Risk ◽  
Peripheral Tissues ◽  
Angiotensin System ◽  
Cerebrovascular Complications ◽  
The Central Nervous System ◽  
Personalized Approach

Since the early days of the pandemic, there have been several reports of cerebrovascular complications during the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Numerous studies proposed a role for SARS-CoV-2 in igniting stroke. In this review, we focused on the pathoetiology of stroke among the infected patients. We pictured the results of the SARS-CoV-2 invasion to the central nervous system (CNS) via neuronal and hematogenous routes, in addition to viral infection in peripheral tissues with extensive crosstalk with the CNS. SARS-CoV-2 infection results in pro-inflammatory cytokine and chemokine release and activation of the immune system, COVID-19-associated coagulopathy, endotheliitis and vasculitis, hypoxia, imbalance in the renin-angiotensin system, and cardiovascular complications that all may lead to the incidence of stroke. Critically ill patients, those with pre-existing comorbidities and patients taking certain medications, such as drugs with elevated risk for arrhythmia or thrombophilia, are more susceptible to a stroke after SARS-CoV-2 infection. By providing a pictorial narrative review, we illustrated these associations in detail to broaden the scope of our understanding of stroke in SARS-CoV-2-infected patients. We also discussed the role of antiplatelets and anticoagulants for stroke prevention and the need for a personalized approach among patients with SARS-CoV-2 infection.

scholarly journals Reversal of hyperglycemic preconditioning by angiotensin II: role of calcium transport

2005 ◽  
Vol 288 (4) ◽  
pp. H1965-H1975 ◽  
Author(s):  
Viktor Pastukh ◽  
Songwei Wu ◽  
Craig Ricci ◽  
Mahmood Mozaffari ◽  
Stephen Schaffer
Keyword(s):  
Oxidative Stress ◽  
Calcium Transport ◽  
Renin Angiotensin System ◽  
Myocardial Cell ◽  
Contractile Dysfunction ◽  
Ang Ii ◽  
Angiotensin System ◽  
Beneficial Effects ◽  
Hypoxia Exposure

Myocardial cell death is an important contributor to the development of diabetic cardiomyopathy. It has been proposed that diabetes-mediated upregulation of the renin-angiotensin system leads to oxidative stress, the trigger for cardiomyocyte death and contractile dysfunction. However, the adverse effect of ANG II on the diabetic heart may extend beyond the development of the cardiomyopathy. ANG II also alters specific modulators of ischemic injury, such as PKC and calcium transport. Therefore, the present study examined the effect of ANG II on hyperglycemic preconditioning, a glucose-mediated condition associated with the elevation of PKC activity and alterations in calcium transport that render the cell resistant to hypoxia. Exposure of the glucose-treated cell to ANG II during the prehypoxic period blocked glucose-mediated cardioprotection. The reversal of hyperglycemic preconditioning was associated with enhanced accumulation of Ca2+ during hypoxia, an effect prevented by inhibition of the Na+/ H+ exchanger and the T-type Ca2+ channel. The inhibitors of hypoxia-mediated Ca2+ accumulation also blocked the reversal of hyperglycemic preconditioning by ANG II. Thus ANG II and glucose treatment exert opposite actions on the Na+/ H+ exchanger and the T-type Ca2+ channel. Because those transporters are involved in hypoxia-mediated apoptosis, they are logical candidates for the beneficial effects of high glucose and the adverse effects of ANG II on the hypoxic cardiomyocyte.

scholarly journals ACE2/ANG-(1–7)/Mas pathway in the brain: the axis of good

2011 ◽  
Vol 300 (4) ◽  
pp. R804-R817 ◽  
Author(s):  
Ping Xu ◽  
Srinivas Sriramula ◽  
Eric Lazartigues
Keyword(s):  
Neurological Diseases ◽  
Renin Angiotensin System ◽  
Transgenic Animals ◽  
Angiotensin Iv ◽  
Angiotensin System ◽  
Angiotensin Converting Enzyme 2 ◽  
Mas Receptor ◽  
Angiotensin Peptides ◽  
The Central Nervous System

The last decade has seen the discovery of several new components of the renin-angiotensin system (RAS). Among them, angiotensin converting enzyme-2 (ACE2) and the Mas receptor have forced a reevaluation of the original cascade and led to the emergence of a new arm of the RAS: the ACE2/ANG-(1–7)/Mas axis. Accordingly, the new system is now seen as a balance between a provasoconstrictor, profibrotic, progrowth axis (ACE/ANG-II/AT1 receptor) and a provasodilatory, antifibrotic, antigrowth arm (ACE2/ANG-(1–7)/Mas receptor). Already, this simplistic vision is evolving and new components are branching out upstream [ANG-(1–12) and (pro)renin receptor] and downstream (angiotensin-IV and other angiotensin peptides) of the classical cascade. In this review, we will summarize the role of the ACE2/ANG-(1–7)/Mas receptor, focusing on the central nervous system with respect to cardiovascular diseases such as hypertension, chronic heart failure, and stroke, as well as neurological diseases. In addition, we will discuss the new pharmacological (antagonists, agonists, activators) and genomic (knockout and transgenic animals) tools that are currently available. Finally, we will review the latest data regarding the various signaling pathways downstream of the Mas receptor.

The Role of Angiotensin-(1-7)/Mas Axis and Angiotensin Type 2 Receptors in the Central Nervous System in Cardiovascular Disease and Therapeutics: A Riddle to be Solved

2019 ◽  
Vol 17 (4) ◽  
pp. 319-325 ◽  
Author(s):  
Vasiliki Katsi ◽  
Spyridon Maragkoudakis ◽  
Maria Marketou ◽  
Costas Tsioufis ◽  
Fragkiskos Parthenakis ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Experimental Studies ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Pressure Lowering ◽  
The Central Nervous System ◽  
Novel Therapeutic Strategies ◽  
Angiotensin Type

: In recent years, the Angiotensin-(1-7)/Mas receptor [Ang-(1-7)/Mas] sub-branch of the Renin-Angiotensin System (RAS) in the brain, and Angiotensin Type 2 Receptors (AT2R), have attracted scientific interest, as there is evidence that they constitute an essential pathway in cardiovascular regulation, in health and in disease. By acting centrally, the Ang-(1-7)/Mas axis - that has been termed ‘the axis of good’- can exert blood pressure-lowering effects, while also favourably altering baroreflex sensitivity and noradrenergic neurotransmission. Thus, research has focused on the possible neuro- and cardioprotective effects of this pathway in the setting of cardiovascular disease, ultimately aiming to evaluate the potential for development of novel therapeutic strategies based on its modulation. : We summarize the available evidence from experimental studies in this context, aiming to assess current limits of scientific knowledge relevant to this newly-described ‘player’ in haemodynamic regulation, that may become a potential therapeutic target.

Role of genetic variability in the renin-angiotensin system in diabetic and nondiabetic renal disease

2001 ◽  
Vol 21 (6) ◽  
pp. 580-592 ◽  
Author(s):  
Arnold Boonstra ◽  
Dick de Zeeuw ◽  
Paul E. de Jong ◽  
Gerjan Navis
Keyword(s):  
Genetic Variability ◽  
Renal Disease ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin
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