Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Table of Contents | Next Article »
Hypertension. 1982;4:3-12

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Berecek, K. H.
Right arrow Articles by Brody, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Berecek, K. H.
Right arrow Articles by Brody, M. J.

Hypertension, Vol 4, 3-12, Copyright © 1982 by American Heart Association

ARTICLES

Vasopressin and vascular reactivity in the development of DOCA hypertension in rats with hereditary diabetes insipidus

KH Berecek, RD Murray, F Gross and MJ Brody

To examine the role of vasopressin (VP) in DOCA-salt hypertension, arterial pressure and renal vascular reactivity were studied in control Long-Evans (LE) rats and in Brattleboro rats homozygous for diabetes insipidus (DI rats). Vascular reactivity to norepinephrine, VP and angiotensin II was assessed in isolated kidneys perfused at constant flow. LE rats showed an increase in arterial pressure (AP) which was significant at 2 weeks post DOCA and averaged 180 mm Hg at 4 weeks. DI rats lacking VP showed no rise in AP after DOCA; however, DI rats given VP and DOCA developed hypertension with a course and magnitude similar to that observed in LE rats. At 6 to 10 weeks post DOCA, renal vascular reactivity to all agents was increased in LE rats and DI rats replaced with VP. Normotensive DI rats lacking VP showed depressed reactivity. Assessment of changes in reactivity at 3 days post DOCA showed that changes preceded the rise in AP. These data suggest that VP may play a primary role in the pathogenesis of DOCA hypertension and that its mechanism may involve an induction of increased vascular reactivity.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
K. Tachikawa, H. Yokoi, H. Nagasaki, H. Arima, T. Murase, Y. Sugimura, Y. Miura, M. Hirabayashi, and Y. Oiso
Altered cardiovascular regulation in arginine vasopressin-overexpressing transgenic rat
Am J Physiol Endocrinol Metab, December 1, 2003; 285(6): E1161 - E1166.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
H. D. Intengan, J. B. Park, and E. L. Schiffrin
Blood Pressure and Small Arteries in DOCA-Salt-Treated Genetically AVP-Deficient Rats : Role of Endothelin
Hypertension, October 1, 1999; 34(4): 907 - 913.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
Y. Hirata, H. Hayakawa, M. Kakoki, A. Tojo, E. Suzuki, D. Nagata, K. Kimura, A. Goto, K. Kikuchi, T. Nagano, et al.
Receptor Subtype for Vasopressin-Induced Release of Nitric Oxide From Rat Kidney
Hypertension, January 1, 1997; 29(1): 58 - 64.
[Abstract] [Full Text]

Home page
 JAMAHome page
R. A. Holden
Alcohol, Nutrient Intake, and Hypertension
JAMA, July 26, 1985; 254(4): 503 - 504.
[Abstract] [PDF]


Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search
Copyright © 1982 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.