Angiotensin type 1A receptors transfected into the A1 neurons inhibit baroreflex gain and the cardiovascular response to stress in AT1A−/− mice

2011 ◽  
Vol 163 (1-2) ◽  
pp. 53
Author(s):  
K. Palma-Rigo ◽  
T.P. Nguyen-Huu ◽  
P.J. Davern ◽  
J.K. Bassi ◽  
J.L. Elghozi ◽  
...  
1996 ◽  
Vol 23 (2) ◽  
pp. 171-176 ◽  
Author(s):  
Joseph A. DiMicco ◽  
Elizabeth H. Stotz-Potter ◽  
Amy J. Monroe ◽  
S Michelle Morin

2001 ◽  
Vol 280 (1) ◽  
pp. R8-R15 ◽  
Author(s):  
Timothy W. Bailey ◽  
Joseph A. Dimicco

The hallmark neuroendocrine response to stress is increased plasma ACTH. Inhibition of neurons in the region of the dorsomedial hypothalamus (DMH) attenuates experimental air stress-induced elevation of heart rate (HR), mean arterial pressure (MAP), and plasma ACTH. We hypothesized that, under basal conditions, stimulation of the DMH would mimic the neuroendocrine and cardiovascular response to air stress. We examined the effects of unilateral microinjection (100-nl vol) of bicuculline methiodide (BMI, 10 pmol), kainate (KA, 1 or 3 pmol), and N-methyl-d-aspartate (5 pmol) into the DMH or the paraventicular nucleus (PVN) on HR, MAP, locomotor activity, and plasma ACTH in conscious rats. Chemical stimulation of the DMH with KA or BMI produced increased locomotor activity and effects on HR, MAP, and plasma ACTH that together mimicked the pattern seen in experimental stress. Similar treatment in the PVN produced only small increases in MAP. Thus activation of neurons in the region of the DMH results in increased secretion of ACTH along with other changes typically seen in experimental stress.


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