scholarly journals AMPK: a balancer of the renin–angiotensin system

2019 ◽  
Vol 39 (9) ◽  
Author(s):  
Jia Liu ◽  
Xuan Li ◽  
Qingguo Lu ◽  
Di Ren ◽  
Xiaodong Sun ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Recent Literature ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Cellular Energy ◽  
Arterial Blood ◽  
Energy Sensor ◽  
Cellular Pathways ◽  
Amp Activated Protein Kinase

Abstract The renin–angiotensin system (RAS) is undisputedly well-studied as one of the oldest and most critical regulators for arterial blood pressure, fluid volume, as well as renal function. In recent studies, RAS has also been implicated in the development of obesity, diabetes, hyperlipidemia, and other diseases, and also involved in the regulation of several signaling pathways such as proliferation, apoptosis and autophagy, and insulin resistance. AMP-activated protein kinase (AMPK), an essential cellular energy sensor, has also been discovered to be involved in these diseases and cellular pathways. This would imply a connection between the RAS and AMPK. Therefore, this review serves to draw attention to the cross-talk between RAS and AMPK, then summering the most recent literature which highlights AMPK as a point of balance between physiological and pathological functions of the RAS.

Terlipressin Versus  Norepinephrine to Correct Refractory Arterial Hypotension after General Anesthesia in Patients Chronically Treated with Renin-Angiotensin System Inhibitors

2003 ◽  
Vol 98 (6) ◽  
pp. 1338-1344 ◽  
Author(s):  
Gilles Boccara ◽  
Alexandre Ouattara ◽  
Gilles Godet ◽  
Eric Dufresne ◽  
Michèle Bertrand ◽  
...  
Keyword(s):  
Blood Pressure ◽  
General Anesthesia ◽  
Arterial Blood Pressure ◽  
Renin Angiotensin System ◽  
Arterial Hypotension ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Long Term Treatment ◽  
Systolic Arterial Blood Pressure

Background Terlipressin, a precursor that is metabolized to lysine-vasopressin, has been proposed as a drug for treatment of intraoperative arterial hypotension refractory to ephedrine in patients who have received long-term treatment with renin-angiotensin system inhibitors. The authors compared the effectiveness of terlipressin and norepinephrine to correct hypotension in these patients. Methods Among 42 patients scheduled for elective carotid endarterectomy, 20 had arterial hypotension following general anesthesia that was refractory to ephedrine. These patients were the basis of the study. After randomization, they received either 1 mg intravenous terlipressin (n = 10) or norepinephrine infusion (n = 10). Beat-by-beat recordings of systolic arterial blood pressure and heart rate were stored on a computer. The intraoperative maximum and minimum values of blood pressure and heart rate, and the time spent with systolic arterial blood pressure below 90 mmHg and above 160 mmHg, were used as indices of hemodynamic stability. Data are expressed as median (95% confidence interval). Results Terlipressin and norepinephrine corrected arterial hypotension in all cases. However, time spent with systolic arterial blood pressure below 90 mmHg was less in the terlipressin group (0 s [0-120 s] vs. 510 s [120-1011 s]; P < 0.001). Nonresponse to treatment (defined as three boluses of terlipressin or three changes in norepinephrine infusion) occurred in zero and eight cases (P < 0.05), respectively. Conclusions In patients who received long-term treatment with renin-angiotensin system inhibitors, intraoperative refractory arterial hypotension was corrected with both terlipressin and norepinephrine. However, terlipressin was more rapidly effective for maintaining normal systolic arterial blood pressure during general anesthesia.

scholarly journals The renin angiotensin system, oxidative stress and mitochondrial function in obesity and insulin resistance

2017 ◽  
Vol 1863 (5) ◽  
pp. 1106-1114 ◽  
Author(s):  
Latha Ramalingam ◽  
Kalhara Menikdiwela ◽  
Monique LeMieux ◽  
Jannette M. Dufour ◽  
Gurvinder Kaur ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Mitochondrial Function ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

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 Alternative renin-angiotensin system pathways in adipose tissue and their role in the pathogenesis of obesity

2016 ◽  
Vol 50 (4) ◽  
pp. 229-240 ◽  
Author(s):  
M Slamkova ◽  
S Zorad ◽  
K Krskova
Keyword(s):  
Insulin Resistance ◽  
Adipose Tissue ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Alternative Pathways ◽  
Metabolism Regulation ◽  
Mas Receptor ◽  
Glucose And Lipid Metabolism

AbstractAdipose tissue expresses all the renin-angiotensin system (RAS) components that play an important role in the adipogenesis, lipid and glucose metabolism regulation in an auto/paracrine manner. The classical RAS has been found to be over-activated during the adipose tissue enlargement, thus elevated generation of angiotensin II (Ang II) may contribute to the obesity pathogenesis. The contemporary view on the RAS has become more complex with the discovery of alternative pathways, including angiotensin-converting enzyme 2 (ACE2)/angiotensin (Ang)-(1-7)/Mas receptor, (pro)renin receptor, as well as angiotensin IV(Ang IV)/AT4 receptor. Ang-(1-7) via Mas receptor counteracts with most of the deleterious effects of the Ang II-mediated by AT1 receptor implying its beneficial role in the glucose and lipid metabolism, oxidative stress, inflammation, and insulin resistance. Pro(renin) receptor may play a role (at least partial) in the pathogenesis of the obesity by increasing the local production of Ang II in adipose tissue as well as triggering signal transduction independently of Ang II. In this review, modulation of alternative RAS pathways in adipose tissue during obesity is discussed and the involvement of Ang-(1-7), (pro)renin and AT4 receptors in the regulation of adipose tissue homeostasis and insulin resistance is summarized.

scholarly journals Intermittent Hypoxia Increases Arterial Blood Pressure in Humans Through a Renin-Angiotensin System-Dependent Mechanism

Hypertension ◽  
2010 ◽  
Vol 56 (3) ◽  
pp. 369-377 ◽  
Author(s):  
Glen E. Foster ◽  
Patrick J. Hanly ◽  
Sofia B. Ahmed ◽  
Andrew E. Beaudin ◽  
Vincent Pialoux ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Intermittent Hypoxia ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Arterial Blood ◽  
Dependent Mechanism

scholarly journals The renin-angiotensin system: a target of and contributor to dyslipidemias, altered glucose homeostasis, and hypertension of the metabolic syndrome

2012 ◽  
Vol 302 (6) ◽  
pp. H1219-H1230 ◽  
Author(s):  
Kelly Putnam ◽  
Robin Shoemaker ◽  
Frederique Yiannikouris ◽  
Lisa A. Cassis
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Angiotensin Receptor Blockers ◽  
Renin Angiotensin System ◽  
Cell Types ◽  
The United States ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Metabolic Syndrome ◽  
Altered Glucose

The renin-angiotensin system (RAS) is an important therapeutic target in the treatment of hypertension. Obesity has emerged as a primary contributor to essential hypertension in the United States and clusters with other metabolic disorders (hyperglycemia, hypertension, high triglycerides, low HDL cholesterol) defined within the metabolic syndrome. In addition to hypertension, RAS blockade may also serve as an effective treatment strategy to control impaired glucose and insulin tolerance and dyslipidemias in patients with the metabolic syndrome. Hyperglycemia, insulin resistance, and/or specific cholesterol metabolites have been demonstrated to activate components required for the synthesis [angiotensinogen, renin, angiotensin-converting enzyme (ACE)], degradation (ACE2), or responsiveness (angiotensin II type 1 receptors, Mas receptors) to angiotensin peptides in cell types (e.g., pancreatic islet cells, adipocytes, macrophages) that mediate specific disorders of the metabolic syndrome. An activated local RAS in these cell types may contribute to dysregulated function by promoting oxidative stress, apoptosis, and inflammation. This review will discuss data demonstrating the regulation of components of the RAS by cholesterol and its metabolites, glucose, and/or insulin in cell types implicated in disorders of the metabolic syndrome. In addition, we discuss data supporting a role for an activated local RAS in dyslipidemias and glucose intolerance/insulin resistance and the development of hypertension in the metabolic syndrome. Identification of an activated RAS as a common thread contributing to several disorders of the metabolic syndrome makes the use of angiotensin receptor blockers and ACE inhibitors an intriguing and novel option for multisymptom treatment.

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