AJP - Regu AJP: Renal Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Regul Integr Comp Physiol 251: R359-R364, 1986;
0363-6119/86 $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 Google Scholar
Google Scholar
Right arrow Articles by Romano, F. D.
Right arrow Articles by Jones, S. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Romano, F. D.
Right arrow Articles by Jones, S. B.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 251, Issue 2 359-R364, Copyright © 1986 by American Physiological Society


ARTICLES

Characteristics of myocardial beta-adrenergic receptors during endotoxicosis in the rat

F. D. Romano and S. B. Jones

The effects of in vivo endotoxin administration on beta-adrenergic receptors in rat ventricle membranes were studied using [3H]dihydroalprenolol as a radioligand. Nonlinear regression analysis of saturation binding indicated one-site binding of antagonist in both control and endotoxic tissues. There was no change in maximum binding or dissociation constant of [3H]dihydroalprenolol at 0.5 or 3 h after endotoxin administration or when the rats were in the agonal stage of shock. Isoproterenol competition studies revealed that there was an increase in the slope of the curve from endotoxic tissues at the agonal stages (0.6 +/- 0.06 vs. 0.91 +/- 0.12, control and endotoxic, respectively, P less than 0.05) and that there was a decrease in affinity for isoproterenol binding. Control binding modeled to a two-state fit, whereas binding to endotoxin-exposed membranes modeled to one state of lower affinity. These data suggest that there is an alteration in receptor-adenylate cyclase coupling, which may account for an attenuation of agonist-stimulated cyclase activity. A modification in the beta-adrenergic receptor may contribute to the decrease in myocardial performance during shock.





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