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


     

Am J Physiol Endocrinol Metab 258: E999-E1005, 1990;
0193-1849/90 $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 Rosen, S. G.
Right arrow Articles by Halter, J. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rosen, S. G.
Right arrow Articles by Halter, J. B.

AJP - Endocrinology and Metabolism, Vol 258, Issue 6 E999-1005, Copyright © 1990 by American Physiological Society

ARTICLES

Beta-adrenergic blockade decreases norepinephrine release in humans

S. G. Rosen, M. A. Supiano, T. J. Perry, O. A. Linares, R. V. Hogikyan, M. J. Smith and J. B. Halter
Department of Medicine, Cornell University Medical College, New York, New York 10021.

Beta-Adrenergic blockade with propranolol (PRP) has been reported to cause an increase in plasma norepinephrine (NE) levels in humans, which suggests that a reflex increase in sympathetic nervous system (SNS) vasoconstrictor tone compensates for the hypotensive effect of beta-adrenergic blockade. However, plasma NE levels are an indirect measure of SNS activity. We have developed a two-compartment model of NE kinetics to estimate NE release into an extravascular compartment as a more comprehensive measure of systemic SNS activity. To determine whether beta-adrenergic blockade alters extravascular NE release, we studied nine healthy subjects during sequential infusions of saline and PRP. During PRP infusion, there was an increase in plasma NE levels [1.03 +/- 0.13 to 1.27 +/- 0.21 (SE) nM; P = 0.05], but the extravascular NE release rate decreased significantly (15.5 +/- 1.6 to 9.2 +/- 1.2 nmol.min-1.m-2, P = 0.0002). The plasma NE concentration increased despite the fall in extravascular NE release rate primarily because the clearance of NE from plasma declined (1.55 +/- 0.08 to 1.18 +/- 0.07 l.min-1.m-2, P = 0.0001); the NE spillover rate into plasma did not change (1.73 +/- 0.18 to 1.75 +/- 0.23 nmol.min-1.m-2, P = 0.89). We conclude that PRP decreases extravascular NE release in humans. Suppression of SNS activity may be an additional mechanism of action of nonselective beta-adrenergic antagonists in humans.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
P. M. Grossman, O. A. Linares, M. A. Supiano, H. Oral, R. H. Mehta, and M. R. Starling
Cardiac-specific norepinephrine mass transport and its relationship to left ventricular size and systolic performance
Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H878 - H888.
[Abstract] [Full Text] [PDF]

Home page
 DiabetesHome page
E. B. Marliss and M. Vranic
Intense Exercise Has Unique Effects on Both Insulin Release and Its Roles in Glucoregulation: Implications for Diabetes
Diabetes, February 1, 2002; 51(90001): S271 - 283.
[Abstract] [Full Text] [PDF]

Home page
 Anesth. Analg.Home page
S. Takeda, T. Tomaru, and Y. Inada
Splanchnic Organ Blood Flow During Calcitonin Gene-Related Peptide-Induced Hypotension With or Without Propranolol in Dogs
Anesth. Analg., June 1, 2000; 90(6): 1275 - 1280.
[Abstract] [Full Text] [PDF]


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