Effect of Age on Angiotensin II Receptors from Rat Brain

1979 ◽  
Vol 57 (s5) ◽  
pp. 111s-113s ◽  
Author(s):  
Claire Baxter ◽  
J. Horvath ◽  
G. Duggin ◽  
D. Tiller

1. Angiotensin II receptor binding was studied in specific regions of rat brain at different ages from birth to 14 weeks. 2. The number of specific angiotensin II receptors increased in all regions during the first 2 weeks of life and then decreased to adult levels. Peak numbers of receptors were up to 10 times the adult numbers. 3. The midbrain and thalamus-hypothalamus had maximum numbers of angiotensin II receptors at 2 weeks of age, whereas the rest of the brain regions had maximum numbers at 1 week. 4. Saralasin-infusion experiments suggested that circulating angiotensin-related peptides could reach brain angiotensin II receptors in 2 week old rats, but not in 6 week old rats. 5. It is postulated that the centrally mediated actions of circulating angiotensin II may be particularly important in the newborn.

1995 ◽  
Vol 18 (3) ◽  
pp. 215-216 ◽  
Author(s):  
Sunghou Lee ◽  
Yi-Sook Jung ◽  
Jaeyang Kong

1991 ◽  
Vol 261 (1) ◽  
pp. R209-R216 ◽  
Author(s):  
K. Tsutsumi ◽  
J. M. Saavedra

Angiotensin II receptor subtypes (AT1 and AT2) were characterized in rat brain by displacement with the specific angiotensin antagonists Du Pont 753 and CGP 42112A, respectively, and quantitative autoradiography. Young (2-wk-old) rats expressed AT1 receptors in selected limbic system areas, structures involved in cardiovascular and fluid regulation, parts of the hippocampal formation, and the choroid plexus. In young rats, AT2 receptors were concentrated in areas involved in control and learning of motor activity, sensory areas, and selected limbic system structures. The cingulate cortex, the molecular layer of the cerebellar cortex, and the superior colliculus contained both AT1 and AT2 receptors. The number of AT1 receptors in most areas of adult (8-wk-old) rats was similar to or even higher than that present in young rats. Conversely, AT2 receptors were always much lower in number in adult animals, and in some areas they were undetectable in adults. Their differential localization and development suggest different functions for the specific angiotensin II receptor subtypes.


1999 ◽  
Vol 69 (5) ◽  
pp. 339-351 ◽  
Author(s):  
Suresh G. Shelat ◽  
Jennifer L. King ◽  
Loretta M. Flanagan-Cato ◽  
Steven J. Fluharty

Peptides ◽  
1981 ◽  
Vol 2 (4) ◽  
pp. 441-444 ◽  
Author(s):  
Francis E. Cole ◽  
Howard L. Blakesley ◽  
Karen A Graci ◽  
Edward D. Frohlich ◽  
Allan A. MacPhee

1994 ◽  
Vol 130 (3) ◽  
pp. 291-296 ◽  
Author(s):  
Xin Gao ◽  
Paddy Phillips ◽  
Brian Oldfield ◽  
Deborah Trinder ◽  
John Risvanis ◽  
...  

Gao X, Phillips P, Oldfield B, Trinder D, Risvanis J, Stephenson J, Johnston C. Androgen manipulation and vasopressin binding in the rat brain and peripheral organs. Eur J Endocrinol 1994;130:291–6. ISSN 0804–4643 It is now widely recognized that there is a sexual dimorphism in the development of arginine vasopressin (AVP) immunoreactivity in certain parts of the brain, and that changes in brain AVP immunoreactivity change with manipulation of androgen status. The aim of this experiment was to determine specifically any AVP receptor changes in response to manipulation of androgen levels using a selective V1 antagonist radioligand. Following castration, plasma testosterone levels fell and AVP immunoreactivity was reduced in the lateral septum and bed nucleus of the stria terminalis. With testosterone supplementation in castrated animals, the immunoreactivity in these regions was restored to a higher degree than in sham-operated animals. Central and peripheral V1 AVP receptor binding (as determined using the selective AVP V1 antagonist radioligand [125I](d(CH2)5,sarcosine7)AVP was not changed in any of the brain regions studied or in liver or kidney membranes from the three groups. This study demonstrates that there is no change in brain AVP receptor binding despite changes in regional AVP immunoreactivity in the brain, and excludes any confounding interaction with changes in oxytocin receptors. P A Phillips, Department of Medicine, The University of Melbourne, Austin Hospital, Heidelberg, Victoria 3084, Australia


1991 ◽  
Vol 548 (1-2) ◽  
pp. 1-8 ◽  
Author(s):  
Robert C. Speth ◽  
Brian P. Rowe ◽  
Kevin L. Grove ◽  
Michelle R. Carter ◽  
David Saylor

1992 ◽  
Vol 55 (5) ◽  
pp. 563-573 ◽  
Author(s):  
Brian P. Rowe ◽  
David L. Saylor ◽  
Robert C. Speth

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