JPET

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by SEVERS, W. B.
Right arrow Articles by CONNOR, J. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by SEVERS, W. B.
Right arrow Articles by CONNOR, J. D.
Journal of Pharmacology And Experimental Therapeutics, Vol. 174, Issue 1, 27-34, 1970
Copyright © 1970 by American Society for Pharmacology and Experimental Therapeutics


A CENTRAL EFFECT OF ANGIOTENSIN: RELEASE OF PITUITARY PRESSOR MATERIAL

WALTER B. SEVERS 1, JOAN SUMMY-LONG 1, JAMES S. TAYLOR 1, and JOHN D. CONNOR 1

1 Department of Pharmacology, The Pennsylvania State University, The Milton S. Hershey Medical Center College of Medicine, Hershey, Pennsylvania

A single injection of angiotensin (0.5 µg) into the lateral ventricle of unanesthetized adult rats elevates mean blood pressure approximately 33 mm Hg. This effect, enhanced by hexamethonium administered peripherally, is inhibited by hexamethonium administered centrally. Phenoxybenzamine pretreatment is also inhibitory. Hypophysectomy reduces central pressor activity approximately 50% and ganglionic blockade abolishes the remaining activity. Lesions in the supraoptic nuclei decrease central pressor activity to the values obtained in hypophysectomized animals. Concomitant with its central pressor effect, angiotensin produces neurogenic thirst which can be markedly inhibited by anticholinergic drugs. These data suggest that angiotensin interacts with central neurons to cause release of antidiuretic hormone and polydipsia which, in the absence of compensatory mechanisms, might produce positive water balance.

Submitted on November 25, 1969
Accepted on March 24, 1970




This article has been cited by other articles:


Home page
HypertensionHome page
J. P. Collister and M. D. Hendel
Role of the Subfornical Organ in the Chronic Hypotensive Response to Losartan in Normal Rats
Hypertension, March 1, 2003; 41(3): 576 - 582.
[Abstract] [Full Text] [PDF]


Home page
ANGIOLOGYHome page
H. Kawabe, O. U. Lopes, K. B. Brosnihan, T. Saruta, and C. M. Ferrario
Angiotensin II Pressor Activity Depends on Medial and Lateral Anterior Hypothalamic Pathways
Angiology, August 1, 1995; 46(8): 641 - 648.
[Abstract] [PDF]


Home page
ScienceHome page
R. Miselis, R. Shapiro, and P. Hand
Subfornical organ efferents to neural systems for control of body water
Science, September 7, 1979; 205(4410): 1022 - 1025.
[Abstract] [PDF]


Home page
ScienceHome page
J. BUGGY, A. E. FISHER, W. E. HOFFMAN, A. K. JOHNSON, and M. I. PHILLIPS
Subfornical Organ: A Dipsogenic Site of Action of Angiotension II
Science, July 28, 1978; 201(4353): 380 - 381.
[PDF]


Home page
ScienceHome page
D. Ganten, J. L. Minnich, P. Grenger, K. Hayduk, H. M. Brecht, A. Barbeau, R. Boucher, and J. Genest
Angiotensin-Forming Enzyme in Brain Tissue
Science, July 2, 1971; 173(3991): 64 - 65.
[Abstract] [PDF]




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
 Molecular Interventions Drug Metabolism and Disposition

Copyright © 1970 by the American Society for Pharmacology and Experimental Therapeutics.