HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Dinçer, U. D. Articles by Altan, V. M. Search for Related Content PubMed PubMed Citation Articles by Dinçer, U. D. Articles by Altan, V. M. Social Bookmarking                What's this?

The Effect of Diabetes on Expression of ß₁-, ß₂-, and ß₃-Adrenoreceptors in Rat Hearts

Ü. Deniz Dinçer, Keshore R. Bidasee, ahika Güner, Ayin Tay, A. Tanju Özçelikay, and V. Melih Altan

From the Department of Pharmacology (Ü.D.D., .G., A.T., A.T.Ö., V.M.A.), Faculty of Pharmacy, University of Ankara, Ankara, Turkey; and the Department of Pharmacology and Toxicology (K.R.B.), Indiana University School of Medicine, Indianapolis, Indiana.

Address correspondence and reprint requests to Dr. V. Melih Altan, Department of Pharmacology, Faculty of Pharmacy, University of Ankara, Tandogan 06100, Ankara, Turkey. E-mail: maltan{at}pharmacy.ankara.edu.tr .

Diabetic hearts exhibit decreased responsiveness to stimulation by ß-adrenoreceptor (ß-AR) agonists. This decrease in activity may be due to changes in expression and/or signaling of ß-AR. Recently we showed that right atrial strips from 14-week streptozotocin (STZ)-induced diabetic rat hearts exhibit decreased responsiveness to ß₁-AR agonist stimulation, but not to ß₂-AR agonist. In the present study, we investigated the effects of long-term diabetes on the expression of cardiac ß₁-, ß₂-, and ß₃-ARs and looked at whether these changes could be restored with insulin treatment. Using reverse transcription-polymerase chain reaction (RT-PCR), PAGE, and Western blot analysis, we found that ß₁-AR mRNA and protein levels decreased by 34.9 ± 5.8 and 44.4 ± 5.8%, respectively, in 14 week-STZ-treated diabetic rat hearts when compared with age-matched controls. On the other hand, mRNA levels encoding ß₂- and ß₃-ARs increased by 72.5 ± 16.6 and 97.3 ± 26.1%, respectively. Although the latter translated into a proportional increase in ß₃-AR protein levels (100.0 ± 17.0%), ß₂-AR protein levels decreased to 82.6 ± 1.1% of control. Insulin treatment for 2 weeks, after 12 weeks of untreated diabetes, partially restored ß₁-AR mRNA and protein levels to 60.1 ± 8.4 and 83.2 ± 5.0%, respectively, of control. Although insulin treatment minimally attenuated the rise in mRNA levels encoding ß₂- and ß₃-ARs, the steady-state levels of these proteins returned to near control values. These data suggest that the decreased responsiveness of diabetic hearts to stimulation of ß-AR agonists may be due to a decrease in ß₁-AR and an increase ß₃-AR expression.

CiteULike

Del.icio.us

Digg

Reddit

Technorati

This article has been cited by other articles:

				R. Germack and J. M. Dickenson Induction of {beta}3-Adrenergic Receptor Functional Expression following Chronic Stimulation with Noradrenaline in Neonatal Rat Cardiomyocytes J. Pharmacol. Exp. Ther., January 1, 2006; 316(1): 392 - 402. [Abstract] [Full Text] [PDF]

				Z.-S. Zhang, H.-J. Cheng, K. Onishi, N. Ohte, T. Wannenburg, and C.-P. Cheng Enhanced Inhibition of L-type Ca2+ Current by {beta}3-Adrenergic Stimulation in Failing Rat Heart J. Pharmacol. Exp. Ther., December 1, 2005; 315(3): 1203 - 1211. [Abstract] [Full Text] [PDF]

				N. Yaras, M. Ugur, S. Ozdemir, H. Gurdal, N. Purali, A. Lacampagne, G. Vassort, and B. Turan Effects of Diabetes on Ryanodine Receptor Ca Release Channel (RyR2) and Ca2+ Homeostasis in Rat Heart Diabetes, November 1, 2005; 54(11): 3082 - 3088. [Abstract] [Full Text] [PDF]

				A. Malhotra, R. Begley, B. P. S. Kang, I. Rana, J. Liu, G. Yang, D. Mochly-Rosen, and L. G. Meggs PKC-{varepsilon}-dependent survival signals in diabetic hearts Am J Physiol Heart Circ Physiol, October 1, 2005; 289(4): H1343 - H1350. [Abstract] [Full Text] [PDF]

				A. Morimoto, H. Hasegawa, H.-J. Cheng, W. C. Little, and C.-P. Cheng Endogenous {beta}3-adrenoreceptor activation contributes to left ventricular and cardiomyocyte dysfunction in heart failure Am J Physiol Heart Circ Physiol, June 1, 2004; 286(6): H2425 - H2433. [Abstract] [Full Text] [PDF]

				K. R. Bidasee, Y. Zhang, C. H. Shao, M. Wang, K. P. Patel, U. D. Dincer, and H. R. Besch Diabetes Increases Formation of Advanced Glycation End Products on Sarco(endo)plasmic Reticulum Ca2+-ATPase Diabetes, February 1, 2004; 53(2): 463 - 473. [Abstract] [Full Text]

				K. R. Bidasee, K. Nallani, Y. Yu, R. R. Cocklin, Y. Zhang, M. Wang, U. D. Dincer, and H. R. Besch Jr. Chronic Diabetes Increases Advanced Glycation End Products on Cardiac Ryanodine Receptors/Calcium-Release Channels Diabetes, July 1, 2003; 52(7): 1825 - 1836. [Abstract] [Full Text] [PDF]

				K. R. Bidasee, U. D. Dincer, and H. R. Besch Jr. Ryanodine Receptor Dysfunction in Hearts of Streptozotocin-Induced Diabetic Rats Mol. Pharmacol., December 1, 2001; 60(6): 1356 - 1364. [Abstract] [Full Text] [PDF]