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 261: R1497-R1506, 1991;
0363-6119/91 $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 Yang, H. M.
Right arrow Articles by Lohmeier, T. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Yang, H. M.
Right arrow Articles by Lohmeier, T. E.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 261, Issue 6 1497-R1506, Copyright © 1991 by American Physiological Society


ARTICLES

Role of angiotensin in ameliorating the renal actions of norepinephrine

H. M. Yang and T. E. Lohmeier
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.

To determine the importance of the arterial pressure effects of angiotensin II (ANG II) on renal function during acute renal adrenergic stimulation, we examined the effects of a 2-h intrarenal arterial infusion of norepinephrine (NE) at 0.1 and 0.25 micrograms.kg-1.min-1 on renal function in five conscious dogs during 1) control conditions, 2) servo-control of renal arterial pressure (RAP) at control levels, and 3) chronic captopril administration. The low rate of NE infusion produced an approximately 20% decrease in glomerular filtration rate (GFR) and renal plasma flow (RPF) and an approximately 8-mmHg increase in RAP in association with an approximately 2.5-fold rise in plasma renin activity (PRA). The high rate of NE infusion produced greater increments in both PRA and RAP and an approximately 50% reduction in GFR and RPF. Neither servo-control of RAP nor captopril administration significantly affected the above renal responses to the low rate of NE infusion. In marked contrast, when increases in RAP (approximately 20 mmHg) were prevented at the high rate of NE infusion by servo-control of RAP, both the PRA and renal responses were enhanced. Furthermore, when RAP was reduced (approximately 25 mmHg) as a result of chronically blocking the renin-angiotensin system with captopril, the renal responses to the high rate of NE infusion were exaggerated even further; in four of five dogs, total renal ischemia occurred in response to NE. These results indicate that ANG II indirectly ameliorates the renal actions of renal adrenergic stimulation by increasing RAP.


This article has been cited by other articles:


Home page
HypertensionHome page
G. A. Reinhart, T. E. Lohmeier, and C. E. Hord Jr
Hypertension Induced by Chronic Renal Adrenergic Stimulation Is Angiotensin Dependent
Hypertension, May 1, 1995; 25(5): 940 - 949.
[Abstract] [Full Text]




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