scholarly journals Opposing tissue-specific roles of angiotensin in the pathogenesis of obesity, and implications for obesity-related hypertension

2015 ◽  
Vol 309 (12) ◽  
pp. R1463-R1473 ◽  
Author(s):  
Nicole K. Littlejohn ◽  
Justin L. Grobe
Keyword(s):  
Energy Balance ◽  
Cardiovascular Health ◽  
Renin Angiotensin System ◽  
Control Mechanisms ◽  
Signaling Mechanism ◽  
Angiotensin System ◽  
Tissue Specific ◽  
Specific Effects ◽  
Health And Disease ◽  
Obesity Hypertension

Metabolic disease, specifically obesity, has now become the greatest challenge to improving cardiovascular health. The renin-angiotensin system (RAS) exists as both a circulating hormone system and as a local paracrine signaling mechanism within various tissues including the brain, kidney, and adipose, and this system is strongly implicated in cardiovascular health and disease. Growing evidence also implicates the RAS in the control of energy balance, supporting the concept that the RAS may be mechanistically involved in the pathogenesis of obesity and obesity hypertension. Here, we review the involvement of the RAS in the entire spectrum of whole organism energy balance mechanisms, including behaviors (food ingestion and spontaneous physical activity) and biological processes (digestive efficiency and both aerobic and nonaerobic resting metabolic rates). We hypothesize that opposing, tissue-specific effects of the RAS to modulate these various components of energy balance can explain the apparently paradoxical results reported by energy-balance studies that involve stimulating, versus disrupting, the RAS. We propose a model in which such opposing and tissue-specific effects of the RAS can explain the failure of simple, global RAS blockade to result in weight loss in humans, and hypothesize that obesity-mediated uncoupling of endogenous metabolic rate control mechanisms can explain the phenomenon of obesity-related hypertension.

scholarly journals Association between Hypomagnesemia, COVID-19, Respiratory Tract and Lung Disease

2021 ◽  
Vol 15 (1) ◽  
pp. 43-45
Author(s):  
Gavino Faa ◽  
Luca Saba ◽  
Daniela Fanni ◽  
Goce Kalcev ◽  
Mauro Carta
Keyword(s):  
Renin Angiotensin System ◽  
Risk Category ◽  
Controlled Trials ◽  
Type I ◽  
Magnesium Supplementation ◽  
Angiotensin System ◽  
Old Adults ◽  
Cd8 T Lymphocytes ◽  
High Risk Category ◽  
Obesity Hypertension

The complexity of COVID-19 is also related to the multiple molecular pathways triggered by SARS-CoV-2, which is able to cause type I pneumocyte death, trigger intravascular coagulation, interfere with the renin-angiotensin system, dysregulate iron metabolism, ending with the insurgence of a cytokine storm which may lead to death. Old adults with obesity, hypertension, and diabetes are among the high-risk category groups more prone to SARS-CoV-2 infection. Magnesium has been reported to play a major role both in physiology and in pathology, particularly in elderly people, regulating cytotoxic functions of natural killer (NK) cells and CD8+ T lymphocytes. In spite of the absence of controlled trials, the possibility of magnesium supplementation for supportive treatment in patients with COVID-19 should be encouraged. This could be useful in all phases of the COVID-19 disease.

The renin–angiotensin system in retinal health and disease: Its influence on neurons, glia and the vasculature

2010 ◽  
Vol 29 (4) ◽  
pp. 284-311 ◽  
Author(s):  
Erica L. Fletcher ◽  
Joanna A. Phipps ◽  
Michelle M. Ward ◽  
Kirstan A. Vessey ◽  
Jennifer L. Wilkinson-Berka
Keyword(s):  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Health And Disease

scholarly journals Nicotine and the renin-angiotensin system

2018 ◽  
Vol 315 (5) ◽  
pp. R895-R906 ◽  
Author(s):  
Joshua M. Oakes ◽  
Robert M. Fuchs ◽  
Jason D. Gardner ◽  
Eric Lazartigues ◽  
Xinping Yue
Keyword(s):  
Cigarette Smoking ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Regulatory Systems ◽  
Health And Disease ◽  
Former Smokers ◽  
New Generation

Cigarette smoking is the single most important risk factor for the development of cardiovascular and pulmonary diseases (CVPD). Although cigarette smoking has been in constant decline since the 1950s, the introduction of e-cigarettes or electronic nicotine delivery systems 10 yr ago has attracted former smokers as well as a new generation of consumers. Nicotine is a highly addictive substance, and it is currently unclear whether e-cigarettes are “safer” than regular cigarettes or whether they have the potential to reverse the health benefits, notably on the cardiopulmonary system, acquired with the decline of tobacco smoking. Of great concern, nicotine inhalation devices are becoming popular among young adults and youths, emphasizing the need for awareness and further study of the potential cardiopulmonary risks of nicotine and associated products. This review focuses on the interaction between nicotine and the renin-angiotensin system (RAS), one of the most important regulatory systems on autonomic, cardiovascular, and pulmonary functions in both health and disease. The literature presented in this review strongly suggests that nicotine alters the homeostasis of the RAS by upregulating the detrimental angiotensin-converting enzyme (ACE)/angiotensin (ANG)-II/ANG II type 1 receptor axis and downregulating the compensatory ACE2/ANG-(1–7)/Mas receptor axis, contributing to the development of CVPD.

Physiological genomic analysis of the brain renin-angiotensin system

2003 ◽  
Vol 285 (3) ◽  
pp. R498-R511 ◽  
Author(s):  
Robin L. Davisson
Keyword(s):  
Genomic Analysis ◽  
Renin Angiotensin System ◽  
Molecular Tools ◽  
American Physiological Society ◽  
Angiotensin System ◽  
Integrative Physiology ◽  
Renin Angiotensin ◽  
Electrolyte Homeostasis ◽  
Health And Disease ◽  
The Brain

The brain renin-angiotensin system (RAS) has long been considered pivotal in cardiovascular regulation and important in the pathogenesis of hypertension and heart failure. However, despite more than 30 years of study, the brain RAS continues to defy explanation. Our lack of understanding of how the brain RAS is organized at the cellular and regional levels has made it difficult to resolve long-sought questions of how ANG II is produced in the brain and the precise mechanisms by which it exerts its actions. A major reason for this is the difficulty in experimentally dissecting the brain RAS at the regional, cellular, and whole organism levels. Recently, we and others developed a series of molecular tools for selective manipulation of the murine brain RAS, in parallel with technologies for integrative analysis of cardiovascular and volume homeostasis in the conscious mouse. This review, based in part on a lecture given in conjunction with the American Physiological Society Young Investigator Award in Regulatory and Integrative Physiology (Water and Electrolyte Homeostasis Section), outlines the physiological genomics strategy that we have taken in an effort to unravel some of the complexities of this system. It also summarizes the principles, progress, and prospects for a better understanding of the brain RAS in health and disease.

Autocrine regulation of internal anal sphincter tone by renin-angiotensin system: comparison with phasic smooth muscle

2005 ◽  
Vol 289 (6) ◽  
pp. G1164-G1175 ◽  
Author(s):  
Márcio A. F. De Godoy ◽  
Satish Rattan
Keyword(s):  
Smooth Muscle ◽  
Anal Sphincter ◽  
Internal Anal Sphincter ◽  
Renin Angiotensin System ◽  
Control Mechanisms ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Autocrine Regulation ◽  
Basal Tone

The myogenic control mechanisms that govern the basal tone in the internal anal sphincter (IAS) are not known. The present studies determined the autocrine regulation of ANG II in the IAS. The studies were performed in the freshly isolated smooth muscle cells (SMC) of the IAS. We determined the presence of ANG II precursor angiotensinogen (Angen), and the enzymes that convert it into ANG II, using functional, molecular biology, and immunocytochemical studies in rats. ANG II levels in the SMC were determined using ELISA. The IAS SMC generate ANG II at a rate severalfold higher than those from the adjoining smooth muscle of rectum (RSM). RT-PCR data show that IAS exclusively expresses significant higher levels of renin, Angen, and angiotensin-converting enzyme (ACE). These data were confirmed using Western blot analyses and immunocytochemistry. In the IAS SMC, H-77 (10 μM; renin inhibitor) and captopril (1 μM; ACE inhibitor) decreased the basal as well as Angen-increased levels of ANG II. The following functional data corroborate the role of renin-angiotensin system (RAS) in the IAS tone. Angen produced concentration-dependent shortening of the IAS SMC that was inhibited by H-77 and captopril. In addition, H-77 or captopril caused a concentration-dependent fall in the IAS tone vs. nontonic tissues. Basal tone in IAS is partially under the autocrine control of cellular RAS evident by the expression of mRNA coding Angen, renin, and ACE and translation to the respective proteins in the SMC.

BBSome: a New Player in Hypertension and Other Cardiovascular Risks

Hypertension ◽  
2021 ◽  
Author(s):  
Yuying Zhao ◽  
Kamal Rahmouni
Keyword(s):  
Cell Membrane ◽  
Vascular Reactivity ◽  
Cardiovascular Health ◽  
Cardiac Development ◽  
Association Studies ◽  
Renin Angiotensin System ◽  
Cardiovascular Risks ◽  
Cellular Processes ◽  
Associated Proteins ◽  
Obesity Hypertension

The BBSome is an octameric protein complex involved in Bardet-Biedl syndrome (BBS), a human pleiotropic, autosomal recessive condition. Patients with BBS display various clinical features including obesity, hypertension, and renal abnormalities. Association studies have also linked the BBS genes to hypertension and other cardiovascular risks in the general population. The BBSome was originally associated with the function of cilia, a highly specialized organelle that extend from the cell membrane of most vertebrate cells. However, subsequent studies have implicated the BBSome in the control of a myriad of other cellular processes not related to cilia including cell membrane localization of receptors and gene expression. The development of animal models of BBS such as mouse lines lacking various components of the BBSome and associated proteins has facilitated studying their role in the control of cardiovascular function and deciphering the pathophysiological mechanisms responsible for the cardiovascular aberrations associated with BBS. These studies revealed the importance of the neuronal, renal, vascular, and cardiac BBSome in the regulation of blood pressure, renal function, vascular reactivity, and cardiac development. The BBSome has also emerged as a critical regulator of key systems involved in cardiovascular control including the renin-angiotensin system. Better understanding of the influence of the BBSome on the molecular and physiological processes relevant to cardiovascular health and disease has the potential of identifying novel mechanisms underlying hypertension and other cardiovascular risks.

Caloric Restriction and Cardiovascular Health: the Good, the Bad, and the Renin-Angiotensin System

Physiology ◽  
2021 ◽  
Vol 36 (4) ◽  
pp. 220-234
Author(s):  
Aline M. A. de Souza ◽  
Carolyn M. Ecelbarger ◽  
Kathryn Sandberg
Keyword(s):  
Caloric Restriction ◽  
Experimental Animal ◽  
Cardiovascular Health ◽  
Population Studies ◽  
Negative Impact ◽  
Renin Angiotensin System ◽  
Cardiovascular Physiology ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Physiological Research

Much excitement exists over the cardioprotective and life-extending effects of caloric restriction (CR). This review integrates population studies with experimental animal research to address the positive and negative impact of mild and severe CR on cardiovascular physiology and pathophysiology, with a particular focus on the renin-angiotensin system (RAS). We also highlight the gaps in knowledge and areas ripe for future physiological research.

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