The use of phenylethanolamine N-methyltransferase inhibitors in elucidating the role of brain epinephrine in the control of cardiovascular function

Author(s):  
Nina Y Liang ◽  
Richard E Tessel ◽  
Ronald T Borchardt ◽  
William C Vincek ◽  
Gary L Grunewald
2013 ◽  
Vol 8 (4) ◽  
pp. 447-454 ◽  
Author(s):  
Hong Kan ◽  
Zhongxin Wu ◽  
Yen-Chang Lin ◽  
Teh-Hsun Chen ◽  
Jared L Cumpston ◽  
...  

2017 ◽  
Vol 51 (3) ◽  
pp. 157-167 ◽  
Author(s):  
I Prieto ◽  
AB Segarra ◽  
M Martinez-Canamero ◽  
M De Gasparo ◽  
S Zorad ◽  
...  

AbstractThe cardiovascular control involves a bidirectional functional connection between the brain and heart. We hypothesize that this connection could be extended to other organs using endocrine and autonomic nervous systems (ANS) as communication pathways. This implies a neuroendocrine interaction controlling particularly the cardiovascular function where the enzymatic cascade of the renin-angiotensin system (RAS) plays an essential role. It acts not only through its classic endocrine connection but also the ANS. In addition, the brain is functionally, anatomically, and neurochemically asymmetric. Moreover, this asymmetry goes even beyond the brain and it includes both sides of the peripheral nervous and neuroendocrine systems. We revised the available information and analyze the asymmetrical neuroendocrine bidirectional interaction for the cardiovascular control. Negative and positive correlations involving the RAS have been observed between brain, heart, kidney, gut, and plasma in physiologic and pathologic conditions. The central role of the peptides and enzymes of the RAS within this neurovisceral communication, as well as the importance of the asymmetrical distribution of the various RAS components in the pathologies involving this connection, are particularly discussed. In conclusion, there are numerous evidences supporting the existence of a neurovisceral connection with multiorgan involvement that controls, among others, the cardiovascular function. This connection is asymmetrically organized.


Hypertension ◽  
2009 ◽  
Vol 54 (3) ◽  
pp. 459-461 ◽  
Author(s):  
Paul D. Chantler ◽  
Edward G. Lakatta

1993 ◽  
Vol 4 (1) ◽  
pp. 39-42 ◽  
Author(s):  
Andrew Thomas

In the sporting world it has become accepted that hard exercise, like running,automatically strengthens the heart and improves circulation. This is a widely held belief and yet one seldom questioned. This article sets out to offer an alternative way of examining the concept of cardiovascular fitness and postulates that exercise may even have an opposite effect. The role of Yoga is then examined.


1987 ◽  
Vol 257 (2) ◽  
pp. 189-207 ◽  
Author(s):  
David A. Ruggiero ◽  
Sima Mraovitch ◽  
Antonio R. Granata ◽  
Muhammad Anwar ◽  
Donald J. Reis

2009 ◽  
Vol 296 (1) ◽  
pp. H13-H28 ◽  
Author(s):  
Boglarka Laczy ◽  
Bradford G. Hill ◽  
Kai Wang ◽  
Andrew J. Paterson ◽  
C. Roger White ◽  
...  

The posttranslational modification of serine and threonine residues of nuclear and cytoplasmic proteins by the O-linked attachment of the monosaccharide β- N-acetylglucosamine ( O-GlcNAc) is a highly dynamic and ubiquitous protein modification. Protein O-GlcNAcylation is rapidly emerging as a key regulator of critical biological processes including nuclear transport, translation and transcription, signal transduction, cytoskeletal reorganization, proteasomal degradation, and apoptosis. Increased levels of O-GlcNAc have been implicated as a pathogenic contributor to glucose toxicity and insulin resistance, which are both major hallmarks of diabetes mellitus and diabetes-related cardiovascular complications. Conversely, there is a growing body of data demonstrating that the acute activation of O-GlcNAc levels is an endogenous stress response designed to enhance cell survival. Reports on the effect of altered O-GlcNAc levels on the heart and cardiovascular system have been growing rapidly over the past few years and have implicated a role for O-GlcNAc in contributing to the adverse effects of diabetes on cardiovascular function as well as mediating the response to ischemic injury. Here, we summarize our present understanding of protein O-GlcNAcylation and its effect on the regulation of cardiovascular function. We examine the pathways regulating protein O-GlcNAcylation and discuss, in more detail, our understanding of the role of O-GlcNAc in both mediating the adverse effects of diabetes as well as its role in mediating cellular protective mechanisms in the cardiovascular system. In addition, we also explore the parallels between O-GlcNAc signaling and redox signaling, as an alternative paradigm for understanding the role of O-GlcNAcylation in regulating cell function.


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