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


     


Am J Physiol Regul Integr Comp Physiol 256: R1308-R1312, 1989;
0363-6119/89 $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 Gruber, K. A.
Right arrow Articles by Callahan, M. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Gruber, K. A.
Right arrow Articles by Callahan, M. F.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 256, Issue 6 1308-R1312, Copyright © 1989 by American Physiological Society


ARTICLES

ACTH-induced hypertension in rats: fact or artifact?

K. A. Gruber, S. L. Eskridge-Sloop, J. C. Eldridge and M. F. Callahan
Department of Medicine, Wake Forest University Medical Center, Winston-Salem, North Carolina 27103.

Evidence from numerous laboratories has shown that administration of adrenocorticotropic hormone (ACTH) to rats produces hypertension within 5 days. However, the analysis of blood pressure in these studies was by the tail-cuff technique, an acute and indirect approach. We have now administered ACTH, via a subcutaneous depot injection (5 or 10 U/day for 9 days), to chronically instrumented rats maintained in metabolic cages. Although tail-cuff measurements of arterial pressure indicated that the ACTH treatment produced hypertension, this was not confirmed by direct 24-h measurements of mean arterial pressure. There was no effect of ACTH on 24-h heart rate throughout the treatment period compared with saline-injected controls. We also examined coefficient of variation of all our measurements. None of the factors was altered by ACTH administration. However, ACTH treatment did produce a diuretic effect, further confirming previous work and providing renal, in addition to cardiovascular, evidence for the bioavailability of the ACTH depot. These results demonstrate that chronic ACTH treatment does not produce a true hypertensive state in rats but rather may enhance the cardiovascular response to the stress of the indirect arterial pressure measurement technique.


This article has been cited by other articles:


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
J. N. Lorenz, E. L. Loreaux, I. Dostanic-Larson, V. Lasko, J. R. Schnetzer, R. J. Paul, and J. B Lingrel
ACTH-induced hypertension is dependent on the ouabain-binding site of the {alpha}2-Na+-K+-ATPase subunit
Am J Physiol Heart Circ Physiol, July 1, 2008; 295(1): H273 - H280.
[Abstract] [Full Text] [PDF]




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