Faculty Opinions recommendation of Imbalance of angiotensin type 1 receptor and angiotensin II type 2 receptor in the rostral ventrolateral medulla: potential mechanism for sympathetic overactivity in heart failure.

2008 ◽  
Author(s):  
Tom Lohmeier
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Potential Mechanism ◽  
Sympathetic Overactivity ◽  
Angiotensin Type

Expression of Angiotensin II Type 1 and Type 2 Receptor in Human Myocardium with Congestive Heart Failure

2000 ◽  
Vol 6 (S2) ◽  
pp. 618-619
Author(s):  
P. Y. Lau ◽  
M. G. Cardarelli ◽  
C. Wei
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Angiotensin Ii ◽  
Cardiac Tissue ◽  
Open Heart Surgery ◽  
Human Myocardium ◽  
Receptor Expression ◽  
At2 Receptors

Angiotensin II (AH) is a potent vasoconstrictor and mitogenic factor. AH receptors include type 1 (ATI) and type 2 (AT2) receptors. Recent studies demonstrated that both ATI and AT2 receptors expressed in human myocardium. Circulating and local tissue level of AH was increased in severe congestive heart failure (CHF). However, the expression of ATI and AT2 in cardiac tissue with CHF remains controversial. Therefore, the present study was designed to investigate the protein expression of ATI and AT2 receptors in normal human myocardium and in human cardiac tissue with mild and severe CHF.Human atrial tissues from normal subjects and CHF patients with ischemic cardiomyopathy and dilated cardiomyopathy were obtained from open-heart surgery and cardiac transplantation. ATI and AT2 receptor expression was investigated by immunohistochemical staining (IHCS). The results of IHCS was evaluated by IHCS staining density scores (0, no staining; 1, minimal staining; 2, mild staining; 3, moderate staining; and 4, strong staining).

scholarly journals Renal Angiotensin Type 2 Receptors Mediate Natriuresis Via Angiotensin III in the Angiotensin II Type 1 Receptor–Blocked Rat

Hypertension ◽  
2006 ◽  
Vol 47 (3) ◽  
pp. 537-544 ◽  
Author(s):  
Shetal H. Padia ◽  
Nancy L. Howell ◽  
Helmy M. Siragy ◽  
Robert M. Carey
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Iii ◽  
Angiotensin Type

scholarly journals Regulation of central angiotensin type 1 receptors and sympathetic outflow in heart failure

2009 ◽  
Vol 297 (5) ◽  
pp. H1557-H1566 ◽  
Author(s):  
Irving H. Zucker ◽  
Harold D. Schultz ◽  
Kaushik P. Patel ◽  
Wei Wang ◽  
Lie Gao
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Transcription Factor ◽  
Critical Role ◽  
Good Evidence ◽  
Receptor Expression ◽  
Ventrolateral Medulla ◽  
Sympathetic Outflow ◽  
Angiotensin Type

Angiotensin type 1 receptors (AT1Rs) play a critical role in a variety of physiological functions and pathophysiological states. They have been strongly implicated in the modulation of sympathetic outflow in the brain. An understanding of the mechanisms by which AT1Rs are regulated in a variety of disease states that are characterized by sympathoexcitation is pivotal in development of new strategies for the treatment of these disorders. This review concentrates on several aspects of AT1R regulation in the setting of chronic heart failure (CHF). There is now good evidence that AT1R expression in neurons is mediated by activation of the transcription factor activator protein 1 (AP-1). This transcription factor and its component proteins are upregulated in the rostral ventrolateral medulla of animals with CHF. Because the increase in AT1R expression and transcription factor activation can be blocked by the AT1R antagonist losartan, a positive feedback mechanism of AT1R expression in CHF is suggested. Oxidative stress has also been implicated in the regulation of receptor expression. Recent data suggest that the newly discovered catabolic enzyme angiotensin-converting enzyme 2 (ACE2) may play a role in the modulation of AT1R expression by altering the balance between the octapeptide ANG II and ANG- (1–7). Finally, exercise training reduces both central oxidative stress and AT1R expression in animals with CHF. These data strongly suggest that multiple central and peripheral influences dynamically alter AT1R expression in CHF.

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