Donate Help Contact The AHA Sign In Home
American Heart Association
Hypertension
Search: search_blue_button Advanced Search
Hypertension. 1982;4:620-624

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 Villamil, M. F.
Right arrow Articles by Taquini, A. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Villamil, M. F.
Right arrow Articles by Taquini, A. C.

Hypertension, Vol 4, 620-624, Copyright © 1982 by American Heart Association


ARTICLES

Role of extracellular volume expansion in the development of DOC-salt hypertension in the rat

MF Villamil, C Amorena, J Ponce-Hornos, A Muller and AC Taquini

Changes in inulin space, plasma and blood volume, exchangeable and "noninulin" sodium were studied during the prehypertensive, early and late hypertensive stages of deoxycorticosterone (DOC)-salt administration in the rat. The effect of an acute water load in previously nephrectomized animals was also studied. Hypertension developed after 1 to 2 weeks of the DOC-salt regimen and was always preceded by enlargement of the inulin space and increased plasma and blood volume. Expansion of extracellular fluids receded when blood pressure started to rise but reappeared after 4 to 6 weeks of treatment. Plasma sodium was high only in the hypertensive groups. An acute water load increased blood pressure of normal rats and decreased blood pressure of DOC-salt early hypertensive rats. These findings suggest that extracellular volume expansion inhibits a vasopressor mechanism that involves vasopressin and could be stimulated by hypernatremia.


This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
M. P. Blaustein, J. Zhang, L. Chen, and B. P. Hamilton
How does salt retention raise blood pressure?
Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2006; 290(3): R514 - R523.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
D. M. Roesch, R. E. Blackburn-Munro, and J. G. Verbalis
Mineralocorticoid treatment attenuates activation of oxytocinergic and vasopressinergic neurons by icv ANG II
Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2001; 280(6): R1853 - R1864.
[Abstract] [Full Text] [PDF]