Diabetes
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
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
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Aronstam, R. S.
Right arrow Articles by Carrier, G. O.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Aronstam, R. S.
Right arrow Articles by Carrier, G. O.
Social Bookmarking
 Add to CiteULike   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

Diabetes, Vol 38, Issue 12 1611-1616, Copyright © 1989 by American Diabetes Association


ARTICLES

Insulin prevention of altered muscarinic receptor-G protein coupling in diabetic rat atria

RS Aronstam and GO Carrier
Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta 30912-2300.

Right atria from rats rendered diabetic by injection of streptozocin (STZ-D) for 8-10 wk are supersensitive to the negative chronotropic effects of muscarinic agonists but have decreased levels of muscarinic receptors and acetylcholinesterase activity. Insulin treatment completely prevents the development of these changes. The proportion of atrial muscarinic receptors displaying high-affinity agonist binding is lower in STZ-D rats; however, the sensitivity of high-affinity agonist binding to regulation by a guanine nucleotide (5'-guanylylimidodiphosphate) is greater in atria from diabetic rats. Again, insulin treatment eliminates these differences. These findings indicate that alterations in atrial muscarinic systems in STZ-D rats are a consequence of the elaboration of the diabetic state and suggest that an alteration of functional muscarinic receptor-G protein coupling contributes to the altered physiological responsiveness of the heart in diabetes.
Add to CiteULike CiteULike   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
J. Appl. Physiol.Home page
K. E. Belmonte, A. D. Fryer, and R. W. Costello
Role of insulin in antigen-induced airway eosinophilia and neuronal M2 muscarinic receptor dysfunction
J Appl Physiol, November 1, 1998; 85(5): 1708 - 1718.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Heart Circ. Physiol.Home page
K. K. Hicks, E. Seifen, J. R. Stimers, and R. H. Kennedy
Diabetes with and without ketoacidosis on right atrial pacemaker rate and autonomic responsiveness
Am J Physiol Heart Circ Physiol, October 1, 1997; 273(4): H1888 - H1893.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Diabetes Diabetes Care Clinical Diabetes Diabetes Spectrum
Copyright © 1989 by the American Diabetes Association.