help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
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 arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Williams, G. H.
Right arrow Articles by Braley, L. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Williams, G. H.
Right arrow Articles by Braley, L. M.

Endocrinology, Vol 98, 1343-1350, Copyright © 1976 by Endocrine Society

ARTICLES

Influence of sodium intake on vascular and adrenal angiotensin II receptors

GH Williams, NK Hollenberg and LM Braley

The restriction of sodium intake reduces the sensitivity of vascular smooth muscle to angiotensin II, but enhances its influence on the adrenal glomerulosa cell. A competitive antagonist to angiotensin II, the Sar1, Ala8 derivative (P113), which shows affinity for the same receptor as angiotensin II, was used to examine the role of receptor affinity in the effect of sodium intake on these two systems in vitro. A threshold P113 concentration reduced the response to angiotensin of aortas derived from rabbits on a high, but not on a low, salt intake. Similarly, a threshold P113 concentration inhibited aldosterone response to angiotensin in glomerulosa cells obtained from sodium- loaded, but not sodium-restricted, rats. Large doses of P113 reduced the response to angiotensin in both preparations on either diet. The competitive antagonist presumably shares affinity for the same receptor on the basis of structural similarities; thus, the results suggest that sodium restriction blunts the vasoactive effects of angiotensin by reducing the affinity of its receptor for angiotensin. In contrast, the enhanced adrenal response to angiotensin with sodium restriction cannot be explained by an altered receptor-agonist interaction, but must reside in a change in an intracellular biochemical process, sufficient to overcome the influence of reduced receptor affinity.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
L. H. Pojoga, T. M. Yao, S. Sinha, R. L. Ross, J. C. Lin, J. D. Raffetto, G. K. Adler, G. H. Williams, and R. A. Khalil
Effect of dietary sodium on vasoconstriction and eNOS-mediated vascular relaxation in caveolin-1-deficient mice
Am J Physiol Heart Circ Physiol, March 1, 2008; 294(3): H1258 - H1265.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
J. S. Williams and G. H. Williams
50th Anniversary of Aldosterone
J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2364 - 2372.
[Full Text] [PDF]

Home page
 HypertensionHome page
N. D. L. Fisher, S. Hurwitz, C. Ferri, X. Jeunemaitre, N. K. Hollenberg, and G. H. Williams
Altered Adrenal Sensitivity to Angiotensin II in Low-Renin Essential Hypertension
Hypertension, September 1, 1999; 34(3): 388 - 394.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 1976 by The Endocrine Society