help button home button Endocrine Society JCEM JCEM Call for Nominations for EIC
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Submit a related Letter to the Editor
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
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 Dalakos, T. G.
Right arrow Articles by Schroeder, E. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dalakos, T. G.
Right arrow Articles by Schroeder, E. T.

Journal of Clinical Endocrinology & Metabolism, Vol 46, 114-118, Copyright © 1978 by Endocrine Society


ARTICLES

Evidence for an angiotensinogenic mechanism of the hypertension of Cushing's syndrome

TG Dalakos, AN Elias, GH Anderson Jr, DH Streeten and ET Schroeder

The blood pressure response to the angiotensin II analog 1-sar-8-ala- angiotensin II, or saralasin, was studied in five patients with clinical and laboratory evidence of Cushing's syndrome. Plasma renin activity, plasma renin substrate, and plasma renin concentration were measured in all five patients. The renin system and the response to saralasin were measured after furosemide administration. Plasma aldosterone was measured after infusion of 2 liters normal saline. All patients studied showed a hypotensive response to saralasin, the mean BP changing from 163/108 mm Hg to 130/85 mm Hg (P less than 0.02). There was a significant elevation of the plasma renin activity and plasma renin concentration in the patients compared to normal subjects, although plasma renin substrate was not significantly different from normal values. There was normal suppression of plasma aldosterone after the infusion of 0.9% saline. The findings indicate that the hypertension of these patients with Cushing's syndrome was mediated in large part by angiotensin II.


This article has been cited by other articles:


Home page
Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
D. A. Scheuer and A. G. Bechtold
Glucocorticoids potentiate central actions of angiotensin to increase arterial pressure
Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2001; 280(6): R1719 - R1726.
[Abstract] [Full Text] [PDF]


Home page
HypertensionHome page
H. Shibata, H. Suzuki, T. Maruyama, and T. Saruta
Gene Expression of Angiotensin II Receptor in Blood Cells of Cushing's Syndrome
Hypertension, December 1, 1995; 26(6): 1003 - 1010.
[Abstract] [Full Text]




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 © 1978 by The Endocrine Society