AJP - Renal Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Renal Physiol 251: F563-F575, 1986;
0363-6127/86 $5.00
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Hamlyn, J. M.
Right arrow Articles by Blaustein, M. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hamlyn, J. M.
Right arrow Articles by Blaustein, M. P.

AJP - Renal Physiology, Vol 251, Issue 4 563-F575, Copyright © 1986 by American Physiological Society

ARTICLES

Sodium chloride, extracellular fluid volume, and blood pressure regulation

J. M. Hamlyn and M. P. Blaustein

Data from humans and experimental animals indicate that hypertensive diseases triggered by extracellular fluid volume expansion are characterized, in their chronic phases, by relatively normal blood volume (BV) and heightened pressure-volume relationship may be viewed as corresponding to a condition of "virtual hypervolemia," where BV is inappropriately "high" relative to blood pressure. The limited data available on the phasic relationship between these variables indicate that the BV expansion appears to be a prerequisite to alterations in vascular ion metabolism, that both of these changes precede the rise in blood pressure, and that structures within the central nervous system may be a critical link between the body fluid volumes and vascular functional changes. In contrast, hypertensive diseases triggered by secretion of pressor agents or their precursors appear to be characterized in their chronic phases by low BV. These relationships and the associated alterations in plasma aldosterone and renin levels are summarized for a variety of clinical syndromes, including essential hypertension and pregnancy-induced hypertension. Direct or indirect evidence of a primary or secondary defect in renal function is apparent as an underlying event in many of these diseases.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
A. C. da Costa Goncalves, R. Leite, R. A. Fraga-Silva, S. V. Pinheiro, A. B. Reis, F. M. Reis, R. M. Touyz, R. C. Webb, N. Alenina, M. Bader, et al.
Evidence that the vasodilator angiotensin-(1 7)-Mas axis plays an important role in erectile function
Am J Physiol Heart Circ Physiol, October 1, 2007; 293(4): H2588 - H2596.
[Abstract] [Full Text] [PDF]

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 HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online