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 254: R56-R60, 1988;
0363-6119/88 $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 Edwards, B. S.
Right arrow Articles by Burnett, J. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Edwards, B. S.
Right arrow Articles by Burnett, J. C., Jr

AJP - Regulatory, Integrative and Comparative Physiology, Vol 254, Issue 1 56-R60, Copyright © 1988 by American Physiological Society

ARTICLES

Role of atrial peptide system in renal and endocrine adaptation to hypotensive hemorrhage

B. S. Edwards, R. S. Zimmerman, T. R. Schwab, D. M. Heublein and J. C. Burnett Jr
Department of Internal Medicine, Mayo Medical School, Rochester, Minnesota 55905.

Hypotensive hemorrhage (HH) is characterized by intravascular volume depletion, avid renal sodium retention, and activation of the renin-angiotensin-aldosterone system (RAAS). The current studies were designed to investigate whether intravascular volume depletion would modulate circulating atrial natriuretic factor (ANF) and, further, to examine what contribution, if any, a decrease in ANF would have in mediating the antinatriuresis and RAAS stimulation associated with HH. Two groups of anesthetized dogs underwent controlled arterial hemorrhage to reduce mean arterial pressure by 15-20 mmHg. Data were collected before and immediately after HH. One group (n = 6) underwent hemorrhage alone, whereas a second group (n = 5) underwent HH with simultaneous administration of alpha-human ANF (2.5 ng.kg-1.min-1), a dose calculated to prevent a reduction in ANF. In the untreated group, circulating ANF was significantly reduced after hemorrhage (79.4 +/- 7.4 to 57.2 +/- 3.4 pg/ml, P less than 0.05), whereas in the treated group ANF increased significantly (73.5 +/- 12.2 to 147.4 +/- 17.2 pg/ml, P less than 0.05). Despite differences in circulating ANF, both groups had similar reductions in urinary sodium excretion and renal blood flow, and similar increases in plasma renin activity. These studies demonstrate that circulating ANF is significantly reduced in HH; however, the mechanism of antinatriuresis and activation of the RAAS is independent of the reduction in circulating ANF.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
V. Frajewicki, L. Kahana, H. Yechieli, V. Brod, R. Kohan, and H. Bitterman
Effects of severe hemorrhage on plasma ANP and glomerular ANP receptors
Am J Physiol Regulatory Integrative Comp Physiol, November 1, 1997; 273(5): R1623 - R1630.
[Abstract] [Full Text] [PDF]


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