scholarly journals Evidence for a histaminergic input from the ventral tuberomammillary nucleus to the solitary tract nucleus involved in arterial pressure regulation

2017 ◽  
Vol 5 (5) ◽  
pp. e13095 ◽  
Author(s):  
Ko Yamanaka ◽  
Sabine S. Gouraud ◽  
Miwa Takagishi ◽  
Akira Kohsaka ◽  
Masanobu Maeda ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Solitary Tract Nucleus ◽  
Pressure Regulation ◽  
Solitary Tract ◽  
Tuberomammillary Nucleus ◽  
Arterial Pressure Regulation

The arterial depressor response to chronic low-dose angiotensin II infusion in female rats is estrogen dependent

2012 ◽  
Vol 302 (1) ◽  
pp. R159-R165 ◽  
Author(s):  
Amanda K. Sampson ◽  
Lucinda M. Hilliard ◽  
Karen M. Moritz ◽  
Merlin C. Thomas ◽  
Chris Tikellis ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Low Dose ◽  
Renin Angiotensin System ◽  
Female Rats ◽  
Ang Ii ◽  
Pressure Regulation ◽  
Estrogen Replacement ◽  
Sprague Dawley ◽  
Arterial Pressure Regulation

The complex role of the renin-angiotensin-system (RAS) in arterial pressure regulation has been well documented. Recently, we demonstrated that chronic low-dose angiotensin II (ANG II) infusion decreases arterial pressure in female rats via an AT2R-mediated mechanism. Estrogen can differentially regulate components of the RAS and is known to influence arterial pressure regulation. We hypothesized that AT2R-mediated depressor effects evident in females were estrogen dependent and thus would be abolished by ovariectomy and restored by estrogen replacement. Female Sprague-Dawley rats underwent ovariectomy or sham surgery and were treated with 17β-estradiol or placebo. Mean arterial pressure (MAP) was measured via telemetry in response to a 2-wk infusion of ANG II (50 ng·kg−1·min−1 sc) or saline. MAP significantly decreased in females treated with ANG II (−10 ± 2 mmHg), a response that was abolished by ovariectomy (+4 ± 2 mmHg) and restored with estrogen replacement (−6 ± 2 mmHg). Cardiac and renal gene expression of components of the RAS was differentially regulated by estrogen, such that overall, estrogen shifted the balance of the RAS toward the vasodilatory axis. In conclusion, estrogen-dependent mechanisms offset the vasopressor actions of ANG II by enhancing RAS vasodilator pathways in females. This highlights the potential for these vasodilator pathways as therapeutic targets, particularly in women.

scholarly journals Balance between cardiac output and sympathetic nerve activity in resting humans: role in arterial pressure regulation

2005 ◽  
Vol 568 (1) ◽  
pp. 315-321 ◽  
Author(s):  
N. Charkoudian ◽  
M. J. Joyner ◽  
C. P. Johnson ◽  
J. H. Eisenach ◽  
N. M. Dietz ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressure Regulation ◽  
Nerve Activity ◽  
Arterial Pressure Regulation
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